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CASE REPORT
Year : 2023 | Volume
: 9
| Issue : 1 | Page : 64-66
Tuberculosis with new onset of diabetes and hypertension following recovery from coronavirus disease 2019 infection: A case series
Rupak Chatterjee1, Aitihya Chakraborty2, Kumkum Sarkar1, Netai Pramanik1, Shatavisa Mukherjee3
1 Department of Tropical Medicine, School of Tropical Medicine, Kolkata, West Bengal, India
2 Department of Microbiology, School of Tropical Medicine, Kolkata, West Bengal, India
3 Department of Clinical and Experimental Pharmacology, School of Tropical Medicine, Kolkata, West Bengal, India
Correspondence Address:
Shatavisa Mukherjee
Department of Clinical and Experimental Pharmacology, School of Tropical Medicine, Kolkata - 700 073, West Bengal
India
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/jpcs.jpcs_14_23
The sign and symptoms of coronavirus disease 2019 (COVID-19) and infectious disease caused by severe acute respiratory syndrome coronavirus 2 are not only restricted to the respiratory system but includes a myriad of clinical manifestations involving various systems. There are various sequelae of COVID-19 reported. Here, we report a series of three cases of tuberculosis along with new onset of diabetes mellitus and hypertension in previously euglycemic, normotensive patients following recovery from COVID-19.
Keywords: Coronavirus disease 2019, diabetes mellitus, hypertension, new onset, tuberculosis
Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), belonging to the family Coronaviridae.[1] Coronaviruses are single-stranded RNA viruses named so due to crown-like spike projections seen on its envelope.[2] COVID-19 presents with various signs and symptoms limited not only to the respiratory system but also to other systems. It is also known to cause multiple sequelae. Here, we report three such cases who were previously normotensive, euglycemic presented to us with exertional shortness of breath or cough following recovery from COVID-19, the cause of which was investigated and found out to be tubercular pleural effusion in two cases and pulmonary tuberculosis (TB) in one case. All three of them also were found to have developed hypertension and diabetes mellitus (DM). COVID-19 pathogenesis and its ability to alter cellular immunity might explain this.
Case ReportsCase 1
A 70-year-old male was admitted with exertional shortness of breath for the last 2 months, aggravated for the last 1 week. Shortness of breath was exacerbated with physical activity. There was no history of postural or diurnal variation of dyspnea. There was no associated history of chest pain and palpitation. Dyspnea was associated with occasional cough with scanty sputum production. He gave an occasional history of low-grade fever. There was no past history of hypertension or diabetes or any history of allergy. No history of addiction was revealed except for occasional smoking. The patient, however, gave a past history of infection with COVID-19, 3 months back with moderate symptoms for which he was admitted and managed conservatively, and then discharged. Since his discharge, he started developing shortness of breath. There was no past or family history of TB.
On examination, his blood pressure was found to be 160/90 mmHg measured on two separate occasions 30 min apart. He had mild pallor and his chest auscultation revealed breath sounds diminished on the right infrascapular region-chest.
On investigation, his complete blood counts showed hemoglobin - 11.9 g%, total leukocyte count − 9300/mm3, neutrophil 86%, lymphocyte - 10%, and platelet – 3.23 lakhs/mm3. His fasting and postprandial blood glucose were 156 md/dl and 213 mg/dl, respectively. Liver function showed albumin - 3 g/dl, globulin - 3.4 g/dl with urea, creatinine, electrolytes, and lipid profile within normal limits. Serum lactate dehydrogenase (LDH) was 494U/l and C-reactive protein-7.4 mg/dl. His chest X-ray (PA) revealed right-sided encysted pleural effusion which was also confirmed by his high-resolution computed tomography thorax [Figure 1] and [Figure 2]. Whole abdomen ultrasound was found normal. His sputum showed growth of Enterobacter cloacae. Urinalysis was observed to be normal. Diagnostic pleural tap revealed 15 cells/mm3 with 95% lymphocytes and no atypical cells. Pleural fluid protein was 4 g/dl, sugar - 125 mg/dl, and LDH-213U/L. Cartridge-based nucleic acid amplification test (CBNAAT) of pleural fluid was positive for Mycobacterium tuberculosis. Gram stain and fungal stain and cultures were negative. Pleural fluid Adenosine Deaminase (ADA) was 38.7U/L. His prior blood reports, i. e., before the time of admission and after discharge for COVID-19 revealed normal blood sugar levels-both fasting and postprandial. His hemoglobin A1C (HbA1c) done during the time of admission in our hospital showed his HbA1c to be 6.5%.
Figure 1: HRCT thorax showing right-sided encysted pleural effusion. HRCT: High-resolution computed tomography
Figure 2: HRCT thorax showing lung parenchymal sections. HRCT: High-resolution computed tomographyHe was started on an antitubercular regimen. He received a course of injection piperacillin/tazobactam and tablet doxycycline for his lower respiratory tract infection. Based on his daily blood pressure measurement and thrice daily capillary blood glucose monitoring during his hospital stay coupled with blood reports, he was diagnosed as a new case of hypertension and diabetes. Managements were given for the same and he was discharged.
Case 2
A 68 years normotensive, non-diabetic female presented with dyspnea with dry cough and low-grade fever and anorexia for 1 month. She had a past history of moderate COVID-19 pneumonia about 8 months back. On clinical examination, she was mildly pale with blood pressure measured as 150/90 mmHg and pulse - 86/min, regular. Chest examination revealed decreased vesicular breath sound in bilateral lung bases. Radiological chest imaging revealed the presence of bilateral mild pleural effusion. Ultrasound-guided diagnostic pleural fluid aspiration was done, which showed lymphocytic predominance in cytology with the exudative nature of the fluid. ADA was 68U/L but CBNAAT was negative. She was treated with antitubercular drugs for 6 months and incentive spirometry for the same. Her fasting and postprandial blood glucose were 135 mg/dl and 232 mg/dl, respectively. She was diagnosed as new-onset hypertension and type 2 DM and oral medications were advised.
Case 3
A 48-year-old male, smoker with 11 pack years of smoking history, nondiabetic, normotensive with past history of COVID-19 pneumonia 6 months back presented with low-grade fever with cough with mild sputum production for 2 months. His blood pressure was measured to be 148/90 mmHg at the time of the outdoor facility visit. His complete blood count showed mild anemia, liver function was within normal limits, and fasting and postprandial blood glucose were 132 mg/dl and 208 mg/dl, respectively. His sputum acid-fast bacilli (AFB) stain revealed plenty of AFB 3+; TrueNat was positive. He was thus diagnosed as sputum-positive pulmonary TB with hypertension and DM and managed accordingly.
In all the above three cases, the patients had normal BP, and their fasting and postprandial blood sugar levels were within the normal range measured or investigated previously at the time of their COVID-19 pneumonia. However, when they presented to us, they were found to meet the criteria for hypertension and DM. Their HbA1c was not such raised but had elevated fasting and postprandial blood glucose levels which indicate diabetes to be of new onset. All of the patients had raised inflammatory cytokine – interleukin 6 levels at baseline of admission and even after 3 months.
DiscussionSARS-CoV-2-like many viruses cause temporary immunosuppressive effects which cause dormant bacterial infections to get reactivated. Lung inflammation and altered type 1 interferon signaling pathway might also be the cause behind the reactivation of dormant TB in the lungs.[3] COVID-19 infection causes temporary suppression of cellular immunity which predisposes to reactivation or new infection with TB.[4] Our patients received a short course of high-dose corticosteroids for COVID-19 management which might have triggered or accelerated mycobacterial growth along with the development of DM and hypertension.
ACE2 receptors, expressed by epithelial cells of lungs, kidneys, intestine, and also blood vessels, play an important role in viral entry into cells.[5] There are hypotheses postulating that ACE2 polymorphisms are linked to SARS-CoV-2 infection and diseases such as diabetes, hypertension, and stroke.[6] COVID-19 infection by causing the release of glucocorticoids and catecholamines in circulation also worsens glycemic control.[7] SARS-CoV-2 might also cause pancreatic injury by direct cytopathic effect and altered harmful immune responses affecting the Islets of Langerhans More Details.[8] There is also downregulation of ACE2 leading to increased angiotensin levels following viral entry to beta cells impairing insulin secretion.[9] The use of corticosteroids in treatment to suppress the inflammation and control cytokine storm might also predispose to diabetes.
Viral angiotensin-converting enzyme 2 (ACE2) binding leads to its downregulation which in turn increases angiotensin II levels which enhances epithelial sodium channel (ENaC) activity. Furthermore, through its effect on the renin–angiotensin–aldosterone system pathway, there is stimulation of aldosterone secretion which augments ENaC activity. Both these factors result in increased sodium reabsorption leading to hypertension.[10]
Hence, it is clear that all the disease conditions discussed above impact each other in terms of progress and outcome. Thus, it is very important to study the effect of these diseases on each other.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Ethics clearance
The study was approved by Institutional Ethics Committee vide Approval No CREC-STM/2022-AS10 dated 06.09.2022.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
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