Lung Involvement Patterns in COVID-19: CT Scan Insights and Prognostic Implications From a Tertiary Care Center in Southern India.

Background COVID-19, caused by the SARS-CoV-2 virus, has presented an unparalleled challenge and a profound learning curve globally. Among the myriad of investigative tools, CT scans of the chest have become instrumental in assessing the magnitude of lung involvement in the pathogenesis of this disease. Objectives This study aimed to evaluate the distribution and patterns of lung involvement depicted in the CT chest scans of COVID-19 patients admitted to a specialized tertiary care center located in a southern state of India. Methods With clearance secured from the Institutional Ethics Committee, an analytical cross-sectional study was conducted. It encompassed CT chest images from all symptomatic COVID-19 patients within the designated study center during the specified study timeline. Subsequent data analysis ensued. Results Among the 1066 COVID-19 patients evaluated, ground-glass opacities (GGO) were the predominant lung involvement pattern. Distinct patterns, such as GGOs combined with solid consolidation or atelectasis, were noted, with the highest mortality linked to GGOs paired with pneumomediastinum (PM). Data underscored a direct correlation between the extent of lung involvement and patient prognosis, with specific lung regions, namely the right apical, right posterior, right superior basal, left superior lingular, and left inferior lingular segments, showing frequent involvement. Conclusion Amidst the pandemic, our study emphasizes that ground-glass opacities on CT scans are robust indicators of COVID-19 in RT-PCR-positive patients. Early identification can enhance patient management, with findings highlighting a strong link between lung involvement and prognosis. This insight aids in refining patient triage, while further research is warranted to delve deeper into variations in lung involvement and guide treatment advancements.

Thyroid Density in CT Imaging as a Potential Marker of Lung Involvement in COVID-19: A Retrospective Analysis.

Background The SARS-CoV-2 pandemic has underscored the multifaceted impact of the virus on human health, extending beyond the respiratory system to involve other organ systems, including the endocrine system. Emerging evidence suggests a notable interaction between COVID-19 and thyroid function, characterized by alterations in thyroid hormone levels and structural changes within the gland. This study aims to explore the association between thyroid density on CT imaging and lung involvement in patients with COVID-19, potentially offering new insights into the systemic effects of the virus. Methodology A retrospective cross-sectional analysis was conducted on 1,066 patients with COVID-19 who underwent chest CT scans without contrast at Government Medical College, Omandurar Government Estate, Chennai, which was designated as the COVID-19 care center from April to June 2021. Thyroid density and lung involvement were quantitatively assessed, and their correlation was analyzed using descriptive and inferential statistics, including the Kruskal-Wallis H test and Shapiro-Wilk test for normality. Results The study population predominantly exhibited normal thyroid density (749, 70.3%), followed by altered (212, 19.9%), nodular (104, 9.8%), and a single instance (0.1%) of absent thyroid density. Despite variability in lung involvement across different thyroid density categories, statistical analysis revealed no significant association between thyroid density and the extent of lung involvement in patients with COVID-19. Conclusions This study found no significant correlation between thyroid density and lung involvement in patients with COVID-19, suggesting that thyroid density on CT imaging may not serve as a reliable marker for lung involvement in this population. Further research is warranted to explore the complex interactions between COVID-19 and thyroid function, as well as the potential implications for patient management and prognosis.

Exploring the Correlation Between Splenomegaly and Lung Involvement in COVID-19: A Retrospective Study.

Background Coronavirus disease 2019 (COVID-19), resulting from the severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), has not only shown substantial effects on the respiratory system but also on extrapulmonary systems, including cardiovascular, gastrointestinal, hematological, and immune responses, notably spleen enlargement. The connection between the enlargement of the spleen and pulmonary complications in individuals with COVID-19 is still not well elucidated, with current studies offering divergent conclusions. Objective This study aims to elucidate the correlation between splenomegaly, as assessed by computed tomography (CT) imaging, and the extent of lung involvement (LI) in COVID-19 patients, thereby offering insights into potential prognostic indicators. Methodology A hospital-based, cross-sectional, retrospective study was conducted involving 1058 symptomatic COVID-19 patients confirmed by reverse transcriptase-polymerase chain reaction (RT-PCR), aged 18 years and above. CT imaging was utilized to evaluate spleen size and LI. Statistical analyses, including Pearson correlation and simple linear regression, were performed to explore the relationship between spleen size and LI. Results The study cohort exhibited a mean spleen size of 9.49 cm and a mean LI score of 0.272. The Pearson correlation coefficient was calculated at 0.0495, indicating a marginal positive correlation between spleen size and LI. Regression analysis demonstrated a minimal impact of spleen size on LI, with spleen size accounting for only 0.2% of the variance in LI scores. Conclusions The study found a slight, statistically non-significant correlation between splenomegaly and LI in COVID-19 patients, suggesting that while splenic enlargement may reflect systemic disease involvement, it is not a strong independent predictor of lung damage extent. The findings highlight the complexity of extrapulmonary manifestations and highlight the need for additional research to fully understand the implications of splenic involvement in COVID-19.

3T proton MR Spectroscopy evaluation of spinal cord lesions.

OBJECTIVE: The objective of this study was to evaluate intramedullary spinal cord lesions using magnetic resonance spectroscopy and correlate the results with histo-pathological examination (HPE). MATERIALS AND METHODS: Approval for this study was obtained from our institute ethical committee. Overall, 50 patients were recruited (29 male and 21 female), with a maximum age of 53 years and minimum age of 7 years. The mean age group of the study was 33 years. Standard magnetic resonance imaging (MRI) spine was done on a Siemens Skyra 3Tesla MRI scanner. MR Spectroscopy (MRS) was performed for all patients with intramedullary spinal lesions after getting written consent. It was performed using single-voxel method. The change in the metabolite peak was observed in each case and the results were compared with HPE. These collected data were analyzed using SPSS 16.0 version. Descriptive statistics, frequency analysis, and percentage analysis were used for categorical variables; and for continuous variables, mean and standard deviation were analyzed. McNemar's test was used to find the significance between conventional MRI MRS. In the above statistical tool, the probability value 0.05 is considered as significant level. RESULTS: From our study, we observed that by applying routine MRI sequences alone, we could only detect around 58% of the cases correctly. However, when MRS was done along with the conventional MR imaging, the number of cases detected significantly increased to 84%. By applying McNemar's test and comparing the conventional MRI and MRS with HPE, it was found that statistically significant difference exists with P value of 0.007. CONCLUSION: MRS of the spinal cord is a promising tool for research and diagnosis because it can provide additional information complementary to other non-invasive imaging methods. It is an emerging tool and adds new biomarker information for characterization of spinal cord tumors, to differentiate benign from malignant lesions and to prevent unnecessary biopsies and surgeries.

Nocturnal hypoglycemia in type 1 diabetes: an assessment of preventive bedtime treatments.

OBJECTIVE: We assessed four putative bedtime treatments in the prevention of nocturnal hypoglycemia in type 1 diabetes. RESEARCH DESIGN AND METHODS: Plasma glucose concentrations were measured every 15 min from 2200 h through 0700 h in 21 patients with type 1 diabetes (mean +/- sd HbA(1C) = 7.1 +/- 1.0%) on five occasions with, in random sequence, bedtime (2200 h) administration of 1) no treatment, 2) a snack, 3) the snack plus the alpha-glucosidase inhibitor acarbose, 4) an uncooked cornstarch bar, or 5) the beta(2)-adrenergic agonist terbutaline. RESULTS: In the absence of a bedtime treatment, 27% of the measured nocturnal plasma glucose concentrations were less than 70 mg/dl (3.9 mmol/liter) in 12 patients; 16, 6, and 1% were less than 60, less than 50, and less than 40 mg/dl (3.3, 2.8, and 2.2 mmol/liter), respectively. Neither the snack (without or with acarbose) nor cornstarch raised the mean nadir nocturnal glucose concentration or reduced the number of low glucose levels or the number of patients with low levels. Terbutaline raised the mean nadir nocturnal glucose concentration (mean +/- se, 127 +/- 11 vs. 75 +/- 9 mg/dl; P < 0.001), eliminated glucose levels less than 50 mg/dl (P = 0.038), reduced levels less than 60 mg/dl (P = 0.005) to one, and reduced levels less than 70 mg/dl (P = 0.001) to five (four at 2215 h, one at 2230 h). However, it also raised glucose levels the following morning. CONCLUSIONS: Nocturnal hypoglycemia is common in aggressively treated type 1 diabetes. Bedtime administration of a conventional snack or of uncooked cornstarch does not prevent it. That of terbutaline prevents nocturnal hypoglycemia but causes hyperglycemia the following morning. The efficacy of a lower dose of terbutaline remains to be determined.

Loss of the decrement in intraislet insulin plausibly explains loss of the glucagon response to hypoglycemia in insulin-deficient diabetes: documentation of the intraislet insulin hypothesis in humans.

The intraislet insulin hypothesis for the signaling of the glucagon secretory response to hypoglycemia states that a decrease in arterial glucose --> a decrease in beta-cell insulin secretion --> a decrease in tonic alpha-cell inhibition by insulin --> an increase in alpha-cell glucagon secretion. To test this hypothesis in humans, a hyperinsulinemic- euglycemic ( approximately 5.0 mmol/l [90 mg/dl] x 2 h) and then a hypoglycemic ( approximately 3.0 mmol/l [55 mg/dl] x 2 h) clamp was performed in 14 healthy young adults on two occasions, once with oral administration of the ATP-sensitive potassium channel agonist diazoxide to selectively suppress baseline insulin secretion and once with the administration of a placebo. The decrement in plasma C-peptide during the induction of hypoglycemia was reduced by approximately 50% in the diazoxide clamps (from 0.3 +/- 0.0 to 0.1 +/- 0.0 nmol/l [0.8 +/- 0.1 to 0.4 +/- 0.1 ng/ml]) compared with the placebo clamps (from 0.4 +/- 0.0 to 0.1 +/- 0.0 nmol/l [1.2 +/- 0.1 to 0.4 +/- 0.1 ng/ml]) (P = 0.0015). This reduction of the decrement in intraislet insulin during induction of hypoglycemia caused an approximately 50% reduction (P = 0.0010) of the increase in plasma glucagon in the diazoxide clamps (from 29 +/- 3 to 35 +/- 2 pmol/l [102 +/- 9 to 123 +/- 8 pg/ml]) compared with the placebo clamps (from 28 +/- 2 to 43 +/- 5 pmol/l [98 +/- 7 to 151 +/- 16 pg/ml]). Baseline glucagon levels, the glucagon response to intravenous arginine, and the autonomic (adrenomedullary, sympathetic neural, and parasympathetic neural) responses to hypoglycemia were not altered by diazoxide. These data indicate that a decrease in intraislet insulin is a signal for the glucagon secretory response to hypoglycemia in healthy humans. The absence of that signal plausibly explains the loss of the glucagon response to falling plasma glucose concentrations, a key feature of the pathogenesis of iatrogenic hypoglycemia, in insulin-deficient (type 1 and advanced type 2) diabetes.

Cortisol elevations comparable to those that occur during hypoglycemia do not cause hypoglycemia-associated autonomic failure.

The concept of hypoglycemia-associated autonomic failure (HAAF) in diabetes posits that recent antecedent iatrogenic hypoglycemia causes both defective glucose counterregulation (by reducing the epinephrine response in the setting of an absent glucagon response) and hypoglycemia unawareness (by reducing the autonomic-sympathetic neural and adrenomedullary response and the resulting neurogenic [autonomic] symptom responses) and thus causes a vicious cycle of recurrent hypoglycemia. To assess the suggestion that it is the cortisol response to antecedent hypoglycemia that mediates HAAF, we tested the hypothesis that plasma cortisol elevations during euglycemia that are comparable to those that occur during hypoglycemia reduce sympathoadrenal and neurogenic symptom responses to subsequent hypoglycemia. To do this, 12 healthy subjects were studied with hyperinsulinemic-stepped hypoglycemic clamps the day after saline or cortisol (1.3 +/- 0.2 micro g. kg(-1) x min(-1)) infusions from 0930 to 1200 and from 1330 to 1600. Compared with saline, antecedent cortisol elevations did not reduce the sympathoadrenal (e.g., final plasma epinephrine levels of 674 +/- 84 vs. 606 +/- 80 pg/ml and final plasma norepinephrine levels of 332 +/- 26 vs. 304 +/- 26 pg/ml) or neurogenic symptom (e.g., final scores of 9.3 +/- 1.1 vs. 13.2 +/- 1.3) responses to subsequent hypoglycemia. Thus, these data do not support the suggestion that cortisol mediates HAAF.

Basal insulin, glucagon, and growth hormone replacement.

Conclusions drawn from the pancreatic (or islet) clamp technique (suppression of endogenous insulin, glucagon, and growth hormone secretion with somatostatin and replacement of basal hormone levels by intravenous infusion) are critically dependent on the biological appropriateness of the selected doses of the replaced hormones. To assess the appropriateness of representative doses we infused saline alone, insulin (initially 0.20 mU.kg(-1).min(-1)) alone, glucagon (1.0 ng.kg(-1).min(-1)) alone, and growth hormone (3.0 ng.kg(-1).min(-1)) alone intravenously for 4 h in 13 healthy individuals. That dose of insulin raised plasma insulin concentrations approximately threefold, suppressed glucose production, and drove plasma glucose concentrations down to subphysiological levels (65 +/- 3 mg/dl, P < 0.0001 vs. saline), resulting in nearly complete suppression of insulin secretion (P < 0.0001) and stimulation of glucagon (P = 0.0059) and epinephrine (P = 0.0009) secretion. An insulin dose of 0.15 mU.kg(-1).min(-1) caused similar effects, but a dose of 0.10 mU.kg(-1).min(-1) did not. The glucagon and growth hormone infusions did not alter plasma glucose levels or those of glucoregulatory factors. Thus, insulin "replacement" doses of 0.20 and even 0.15 mU.kg(-1).min(-1) are excessive, and conclusions drawn from the pancreatic clamp technique using such doses may need to be reassessed.

Maintenance of the postabsorptive plasma glucose concentration: insulin or insulin plus glucagon?

The prevalent view is that the postabsorptive plasma glucose concentration is maintained within the physiological range by the interplay of the glucose-lowering action of insulin and the glucose-raising action of glucagon. It is supported by a body of evidence derived from studies of suppression of glucagon (and insulin, among other effects) with somatostatin in animals and humans, immunoneutralization of glucagon, defective glucagon synthesis, diverse mutations, and absent or reduced glucagon receptors in animals and glucagon antagonists in cells, animals, and humans. Many of these studies are open to alternative interpretations, and some lead to seemingly contradictory conclusions. For example, immunoneutralization of glucagon lowered plasma glucose concentrations in rabbits, but administration of a glucagon antagonist did not lower plasma glucose concentrations in healthy humans. Evidence that the glycemic threshold for glucagon secretion, unlike that for insulin secretion, lies below the physiological range, and the finding that selective suppression of insulin secretion without stimulation of glucagon secretion raises fasting plasma glucose concentrations in humans underscore the primacy of insulin in the regulation of the postabsorptive plasma glucose concentration and challenge the prevalent view. The alternative view is that the postabsorptive plasma glucose concentration is maintained within the physiological range by insulin alone, specifically regulated increments and decrements in insulin, and the resulting decrements and increments in endogenous glucose production, respectively, and glucagon becomes relevant only when glucose levels drift below the physiological range. Although the balance of evidence suggests that glucagon is involved in the maintenance of euglycemia, more definitive evidence is needed, particularly in humans.

Mechanism, temporal patterns, and magnitudes of the metabolic responses to the KATP channel agonist diazoxide.

To assess the mechanism, temporal patterns, and magnitudes of the metabolic responses to the ATP-dependent potassium channel agonist diazoxide, neuroendocrine and metabolic responses to intravenous diazoxide (saline, 1.0 and 2.0 mg/kg) and oral diazoxide (placebo, 4.0 and 6.0 mg/kg) were assessed in healthy young adults. Intravenous diazoxide produced rapid, but transient, decrements (P = 0.0023) in plasma insulin (e.g., nadirs of 2.8 +/- 0.5 and 1.8 +/- 0.3 microU/ml compared with 7.0 +/- 1.0 microU/ml after saline at 4.0-7.5 min) and C-peptide (P = 0.0228) associated with dose-related increments in plasma glucose (P = 0.0044) and serum nonesterified fatty acids (P < 0.0001). After oral diazoxide, plasma insulin appeared to decline, as did C-peptide, again associated with dose-related increments in plasma glucose (P < 0.0001) and serum nonesterified fatty acids (P = 0.0141). Plasma glucagon, as well as cortisol and growth hormone, was not altered. Plasma epinephrine increased (P = 0.0215) slightly only after intravenous diazoxide. There were dose-related increments in plasma norepinephrine (P = 0.0038 and P = 0.0005, respectively), undoubtedly reflecting a compensatory sympathetic neural response to vasodilation produced by diazoxide, but these would not raise plasma glucose or serum nonesterified fatty acid levels. Thus selective suppression of insulin secretion, without stimulation of glucagon secretion, raised plasma glucose and serum nonesterified fatty acid concentrations. These findings define the temporal patterns and magnitudes of the metabolic responses to diazoxide and underscore the primacy of regulated insulin secretion in the physiological regulation of postabsorptive carbohydrate and lipid metabolism.