The effect of COVID-19 on Ramadan fasting in people with diabetes in East London 2020: The East London diabetes in Ramadan survey.

AIMS: Fasting during the COVID-19 crisis was challenging for Muslim people with diabetes during Ramadan. We aimed to survey the experiences of patients with Type 2 diabetes (T2D) during Ramadan 2020. METHODS: Telephone survey of Muslim patients with T2D in Tower Hamlets, London. Patients were surveyed on the effects of COVID-19 on their fast, discussions with a healthcare professional (HCP) before Ramadan, whether they followed advice, number of fasts undertaken, medication changes and adverse events. RESULTS: 829 participated. 334 (40.2%) discussed fasting with a HCP; 198 (59.3%) were advised not to fast; 171 (86.3%) elected not to fast. 12 (1.4%) were admitted to hospital during Ramadan - one fasting related severe hypoglycaemia, one non-fasting cerebrovascular accident, and 10 (four fasting and six non-fasting) with COVID-19 symptoms. 34 (8.2%) patients in the fasting group developed COVID-19 symptoms before or during Ramadan; 30 (7.2%) in the non-fasting cohort. 311 (37.5%) patients said COVID-19 had significantly influenced their decision not to fast. Compared to Ramadan 2016, in Ramadan 2020 fewer people fasted (50.1% vs 55.4%), fewer people discussed fasting with a HCP (40.2% vs 52%), more patients who discussed fasting with their HCP were advised not to fast (59.3% vs 33.8%), and fewer patients fasted against medical advice (13.7% vs. 19.3%). CONCLUSIONS: COVID-19 had an impact on people with diabetes and their fasting intentions during Ramadan 2020. Most people who were advised not to fast did not fast; there were few adverse outcomes from fasting. COVID-19 was not more common amongst people who fasted.

Impact of lockdown in COVID 19 on glycemic control in patients with type 1 Diabetes Mellitus.

BACKGROUND AND AIMS: COVID 19 is a novel pandemic affecting globally. Although no reliable data suggests that patients of well controlled Type 1 Diabetes Mellitus (T1DM) being at increased risk of becoming severely ill with SARS-CoV2, but lockdown may impact patients with T1DM requiring regular medications and follow up. Hence this study was planned to see the impact of lockdown on glycemic control in patients with T1DM. METHODS: A cross sectional study was done in T1DM patients in whom a structured questionnaire was administered on follow up within 15 days after lockdown. Data regarding hypoglycemic and hyperglycemic episodes, Diabetic ketoacidosis (DKA), insulin dose missed, regular glucose monitoring, dietary compliance, physical activity, hospitalization during the phase of lockdown was taken. Average blood glucose and HbA1C of lockdown phase was compared with the readings of prelockdown phase. RESULTS: Out of 52 patients, 36.5% had hyperglycemic and 15.3% had hypoglycemic episodes. Insulin dose was missed in 26.9%, glucose monitoring not done routinely in 36.5% and 17.4% were not diet compliant during lockdown. Average blood glucose during lockdown phase was 276.9 ± 64.7 mg/dl as compared to 212.3 ± 57.9 mg/dl during prelockdown phase. Mean HbA1c value of lockdown (10 ± 1.5%) which was much higher that of pre lockdown (8.8 ± 1.3%) and the difference was statistically significant (p < 0.05). CONCLUSION: Glycemic control of T1DM patients has worsened mainly due to non availability of insulin/glucostrips during lockdown period. There is a need for preparedness in future so that complications can be minimised.

Hypoglycemia at the time of Covid-19 pandemic.

BACKGROUND: Hypoglycemia is the limiting factor in the glycemic management of diabetes, which need to be addressed critically to avoid complications. Lockdown because of new coronavirus strain (COVID-19) pandemic has further complicated the issue of hypoglycemia due to limitations in access to food, outpatient clinics, pathological services and medicines. AIM: To assess the factors associated with the risk of hypoglycemia during April-May 2020 lockdown in people with type 2 diabetes mellitus. METHODOLOGY: We analyzed the data retrospectively from 146 patients of type 2 diabetes mellitus (T2DM) reporting to the emergency department (ED) during lockdown period with symptoms suggestive of hypoglycemia. RESULTS: The majority of patients were male (90/146) with a mean age of 59.88 ± 10.09 years and a mean random blood glucose level of 57.67 ± 9.00 mg/dL. Two-third of patients (70.83%) had level 1 hypoglycemia, while level 2 hypoglycemia was reported in 29.16% of patients. A combination of Metformin and Sulfonylureas (SU) was most commonly associated with the risk of hypoglycemia (65.75%) followed by insulin (33.56%). Subjects who received insulin reported a lower blood glucose value (50.75 ± 8.20 mg/dL) as compared to those receiving a combination of metformin and SU (60.95 ± 7.10 mg/dl). 330.56% of patients who had received prophylaxis hydroxychloroquine (HCQ) 400 mg twice a day along with the routine anti-hyperglycemic agents without their dose adjustment reported hypoglycemia. Patients with hypertension, micro-vascular, macro-vascular complications, and coexistent with each other had a higher propensity to the risk of hypoglycemia (46.58%, 33.56%, 23.29%, and 32.88%) respectively. CONCLUSION: The COVID-19 lockdown has shown to influence the risk of hypoglycemia in patients with T2DM, especially those receiving SU, insulin, HCQ especially in patients with associated co-morbidities. Patient education, support, and telemedicine plays a pivotal role to prevent hypoglycemia.

Manifestations of three HHV-8-related diseases in an HIV-negative patient: immunoblastic variant multicentric Castleman's disease, primary effusion lymphoma, and Kaposi's sarcoma.

We describe a 73-year-old HIV negative patient who presented with symptomatic hypoglycemia. Over the course of several months she was diagnosed with three human herpesvirus-8 related diseases: multicentric Castleman's disease, primary effusion lymphoma and Kaposi's sarcoma. No improvement was observed following cytotoxic therapy and she died 16 months after her initial presentation. The etiology of the hypoglycemia remained obscure over the course of this patient's disease. This case is the first report of a patient with three human herpesvirus-8 related diseases, and the first report of severe hypoglycemia as the presenting symptom of any of these diseases.

A single amino acid change in the glycoprotein of lymphocytic choriomeningitis virus is associated with the ability to cause growth hormone deficiency syndrome.

Persistent infection of C3H/St mice with certain strains of lymphocytic choriomeningitis virus (LCMV) causes a growth hormone (GH) deficiency syndrome (GHDS) manifested as growth retardation and hypoglycemia. Infected mice show high levels of viral replication in the GH-producing cells in the anterior pituitary leading to decreased synthesis of GH mRNA and protein despite the absence of detectable virus-induced cell structural damage. Virus clones isolated from the GHDS-negative LCMV WE strain can cause the disease, while others cannot. The genetic basis of this phenotypic difference is a nucleotide substitution resulting in a single amino acid difference in the viral glycoprotein. Reassortant studies indicate that the single amino acid substitution (Ser-153 to Phe) is sufficient to allow infection of the GH-producing cells and cause GHDS. These results show that a single change in the genome can affect viral pathogenicity by altering the tropism of the virus.

Variants able to cause growth hormone deficiency syndrome are present within the disease-nil WE strain of lymphocytic choriomeningitis virus.

Persistent infection of C3H/St mice with lymphocytic choriomeningitis virus (LCMV) strain Armstrong leads to disordered growth and hypoglycemia. Both host and viral determinants contribute to this growth hormone (GH) deficiency syndrome (GHDS). Development of the GHDS correlates with the virus's ability to replicate in the GH-producing cells and cause reduced levels of GH synthesis. LCMV strain WE infects few GH-producing cells and does not cause GHDS in C3H/St mice. We show here that clonal variants isolated from the GHDS-nil WE population are able to replicate at high levels in GH-producing cells and cause GHDS in C3H/St mice. These variants are stably maintained, but phenotypically silent, within the GHDS-nil WE population.