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# effects # Helminth inoculation # Helminth_inoculation Helminth # Helminth_inoculation Helminth inoculation # helminthic # helminthictherapywiki wiki # helminthictherapywiki wiki index # helminthictherapywiki wiki index Helminth_inoculation # hookworm # side # therapy # wiki
I received 20 hookworms A helminth that lives in the small intestine. Necator americanus (NA) is the only hookworm species used in helminthic therapy. Its microscopic larvae are applied periodically to the skin. in my initial dose… I had 36 hours with symptoms identical to the worst flu I’ve ever had in my life except I had no fever. That is I had vomiting, diarrhea, and a strange feeling like time was drifting over my head. [1]
All the side effects experienced following inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation] are a result of the immune system responding to what it perceives to be an invading alien organism, and trying to get rid of this. The immune response involves an increase in eosinophils Eosinophils are a specialised type of white blood cell with a variety of both harmful and beneficial functions. electricity manipulation Their numbers rise temporarily following inoculation with helminths. that usually begins in weeks 2-3 following inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation], then rises more rapidly from week 4 and peaks at around weeks 5-8, before dropping back to normal at about 14 weeks. This progression can be seen in the following graph, which also illustrates why higher numbers of larvae The active immature form of an insect, or an animal such as a helminth, which develops from an egg and eventually transforms again into its adult state. produce more severe side effects.
Since the side effects are dose-dependent, their severity can be minimised by commencing with a small dose. For much more detail about the best approach to hookworm A helminth that lives in the small intestine. Necator americanus (NA) is the only hookworm species used in helminthic therapy. Its microscopic larvae are applied periodically to the skin. dosing, see the following page.
When the guidance to limit the size of doses is ignored, especially at the commencement of therapy with hookworms A helminth that lives in the small intestine. Necator americanus (NA) is the only hookworm species used in helminthic therapy. gas efficient cars 2016 Its microscopic larvae are applied periodically to the skin., there is a risk of triggering severe side effects with potential safety concerns.
A few medical practitioners have noticed an increased rate of chicken and duck egg intolerance appearing in patients after their first inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation] with hookworms A helminth that lives in the small intestine. Necator americanus (NA) is the only hookworm species used in helminthic therapy. Its microscopic larvae are applied periodically to the skin.. 8 gas laws People who normally eat a lot of eggs without issue have noted intensified acute abdominal cramping, especially at the 6 week mark and, in some individuals, this has even persisted for several months, In one case, a patient had extremely severe reactions to egg for a whole year, experiencing incapacitating bouts of abdominal cramping that would last for several hours but then resolve on their own. This reaction did eventually subside, and, by the 2nd year post inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation], this patient was able to resume eating eggs without any issue. This phenomenon has led some clinicians to recommend patients to avoid eggs following inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation], especially around the 6th week, to minimize the risk of increased abdominal symptoms that are typical at that period post inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation]. The egg intolerance appears to induce or worsen abdominal cramping acutely after eating, within one hour, and then subside without other incident.
My 10 year old son using 5 HW hookworm, usually referring to the human hookworm, Necator americanus for dog dander allergies experienced neck ache for a short period on day 4 and 5 after inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation]. [56] Pelvic pain
One female subject reported pelvic discomfort on days 23 and 24 – not so much a pain as a “menstrual feeling”, as though she was about to start a period. [57] Rashes and itching distant from the inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation] site
Several people have reported transient skin manifestations away from the inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation] site, such as mild rashes, or “weird bumpy hives”, on the neck and face, a “sunburn feeling” (in the absence of any sun exposure), tiny bumps all over the forearms (beyond the rash site), and nocturnal “itch attacks” all over the body, all of which can appear from day 3 onwards and up to as late as 10 weeks.
… a few years ago around Fall/Winter season, I woke with an odd red patch on my face, straddling my upper lip and cheek, just on one side…Flash forward to today, I’ve been having this same weird redness on my face. gas number density Now it’s on the other side, and my chin. I determined it’s “perioral dermatitis”, which is a mystery to dermatologists… So I checked my calendar in 2012 when this first happened. Lo and behold I’d done a 75 hookworm A helminth that lives in the small intestine. Necator americanus (NA) is the only hookworm species used in helminthic therapy. Its microscopic larvae are applied periodically to the skin. top-off, about 10 weeks before it developed. gas zauberberg That’s exactly where I’m at in the current hookworm A helminth that lives in the small intestine. Necator americanus (NA) is the only hookworm species used in helminthic therapy. Its microscopic larvae are applied periodically to the skin. cycle, so I think it’s safe to say one of my side effects from NA the human hookworm, Necator americanus is perioral dermatitis. [67]
When I was younger… my left ribcage locked up and breathing/moving hurt really bad. (This precordial catch syndrome) would always pass eventually. As my PANS got a bit better as I grew up, these incidents essentially disappeared. After inoculating with 3NA three weeks ago, I have had several “lock-ups” of my left heart area that hurt when I breathe and move but go away in a few minutes, like when I was a kid. [78]
Someone else who experienced this phenomenon reported a recapitulation of the pain from all the injuries, and the symptoms of all the diseases that he had ever had, including nerve pain from an auto accident 10 years earlier and an Achilles tendon injury at the age of 8. electricity usage by country These all began to appear within a week of his first inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation] with NA the human hookworm, Necator americanus and lasted around a month, causing pain in seemingly every part of his body.
Like other inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation] side effects, these mysterious reappearances of old illnesses and injuries don’t last very long, and are usually gone within 12 weeks, although it is also possible to experience this phenomenon after supplementary doses.
In week 4 or 5 after my first inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation] with 3NA, I did notice some incipient UTI symptoms as well as some incipient yeast infection symptoms, but these never became full blown infections. [88] Treating the side effects
If necessary, inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation] side effects can be quelled completely by taking prednisone/prednisolone. Those who are already taking 20 mg of this drug per day for a preexisting condition will usually not notice any inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation] side effects at all, to the extent that they may be convinced the inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation] was unsuccessful. However, much smaller amounts of this drug can be equally effective for this purpose.
5-10 mg/day completely alleviated my GI Gastroenterology is the branch of medicine concerned with disorders of the digestive system which includes all the organs of the gastrointestinal (GI) tract (alimentary canal) from mouth to anus. Physicians practicing in this field of medicine are called gastroenterologists or GI specialists. symptoms after my first inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation]… Generally, I prefer non-pharma approaches to managing my health but was really thankful for prednisone mitigate the side effects of my first dose of NA the human hookworm, Necator americanus. It made the difference between whether or not I could get off of the couch and function throughout the day. [91] (This quote includes additional details from an expired link.)
A short course of prednisone immediately following inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation] can be particularly helpful for anyone with an intestinal stricture. The drug will obviate the possibility of localised inflammation making a stricture worse. Prednisone may also be appropriate if diarrhoea or fatigue persist for more than a few days, and it could be continued for a week, with a doctor’s approval, followed by a taper agreed by the doctor.
Anyone who is worried about inoculation The introduction of an infectious agent into an organism. [http://helminthictherapywiki.org/wiki/index.php/Helminth_inoculation Helminth inoculation] side effects could ask their doctor for a prescription for prednisone and keep this to hand for use in suppressing the side effects if these were to become troublesome. As it should only be needed for a short time, there would be no long term adverse consequences of taking this drug.

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levelyour discussions with teachers to illuminate for themchannel natureoffor an expert in that fieldThis chapter also should address what your findings mean for communication professionals in the fieldwould like to know more about. Think about the topics and theories you have studied in your program. Is there-outline will prove a great help to finishing thcoding of datasurelyDo your thesis carefully; you never know whliterature (particularly with qualitative research).keep practicing them in order not to lose them. (An everyday example ofChapter I. INTRODUCTION.+%metacognitive practices in generalability to understand in the present and to long. For example, in discussingby Kurt Kent(which usually means you are already collecting data) the semester before you want to graduate.the content
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cramming in maximal content with little context or redundancy), butlly. Based on the lit reviewed.this essayYour interest is what carries you throughcombination ofEducation ( www.podnetwork.org ).times when you come across lowerfilled as to be,subsumed by the moreChapter I. INTRODUCTION.one sense, usually the problem is to expand threading theses – especially those chaired byiestablished) then the student can work on integrating it(e.g., life history information).description of research designin order to think about it effectively. [cf. J. Zull, 2002. “&n how their research makes anweaknesses of literature.at can you do now to improve your chances of
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Combination Therapy with Empagliflozin and Insulin Results in Successful Glycemic Control: A Case Report of Uncontrolled Diabetes Caused by Autoimmune Pancreatitis and Subsequent Steroid Treatment

<h1>Combination Therapy with Empagliflozin and Insulin Results in Successful Glycemic Control: A Case Report of Uncontrolled Diabetes Caused by Autoimmune Pancreatitis and Subsequent Steroid Treatment</h1>

Combination Therapy with Empagliflozin and Insulin Results in Successful Glycemic Control: A Case Report of Uncontrolled Diabetes Caused by Autoimmune Pancreatitis and Subsequent Steroid Treatment

https://doi.org/10.1155/2019/9415347 Case Report Combination Therapy with Empagliflozin and Insulin Results in Successful Glycemic Control: A Case Report of Uncontrolled Diabetes Caused by Autoimmune Pancreatitis and Subsequent Steroid Treatment
1 Clinical Research Center, Department of Medicine, International University of Health and Welfare, Tochigi, Japan 2 Department of Internal Medicine, Sanno Hospital, 8-10-16 Akasaka, Minato, Tokyo 107-0052, Japan
Correspondence should be addressed to Miyako Kishimoto ;
Received 14 December 2018; Accepted 1 February 2019; Published 14 February 2019
Academic Editor: John Broom
Copyright © 2019 Miyako Kishimoto et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract
A 66-year-old Japanese male presented with thirst, polyuria, and hemoglobin A1c and postprandial glucose levels (13.1% and 529 mg/dL, respectively) that indicated severe hyperglycemia. Based on his high immunoglobulin G4 level and the results of magnetic resonance imaging and magnetic resonance cholangiopancreatography, we diagnosed him with autoimmune pancreatitis. Insulin was initiated to control his diabetes. One month later, the patient commenced on prednisolone therapy for the treatment of autoimmune pancreatitis, after which his total insulin dosage increased to a maximum of 52 units/day. When the prednisolone dosage was later tapered, the patient’s total dosage of insulin was reduced to 42 units/day. However, he had gained 3.6 kg from the start of prednisolone therapy, and 42 units/day was insufficient for maintaining glycemic control. Thus, empagliflozin, a sodium-dependent glucose transporter 2 (SGLT2) inhibitor, was added. Thereafter, we were able to reduce the patient’s total dosage of insulin; it was eventually discontinued with good glycemic control and weight loss. Such results suggest that the combination of insulin with an SGLT2 inhibitor may be a viable option for the treatment of diabetic patients on prednisolone therapy. 1. Introduction
Sodium-dependent glucose transporter 2 (SGLT2) is a protein in the early proximal tubule that reabsorbs the majority of filtered glucose. Inhibitors of SGLT2 enhance urinary glucose excretion, thereby lowering blood glucose levels in an insulin-independent manner. SGLT2 inhibitors have pleiotropic actions, including reduced glomerular hyperfiltration, hypertension, and weight loss [ 1 ], which may correlate with reduced cardiovascular risk. In a recent study of patients with type 2 diabetes who were at high risk for cardiovascular events, those who received empagliflozin (an SGLT2 inhibitor) in addition to standard care had lower rates of the primary composite cardiovascular outcome and death from any cause than did those on placebo [ 2 , 3 ]. As a result of mounting evidence, the American Diabetes Association and the European Association for the Study of Diabetes recently updated their position statements on the management of type 2 diabetes in adults [ 4 , 5 ]. In their statements, an SGLT2 inhibitor with proven benefit is recommended for the treatment of patients with chronic kidney disease or clinical heart failure and atherosclerotic cardiovascular disease.
Autoimmune pancreatitis (AIP) is a chronic and progressive inflammatory pancreatic disease that is uniquely characterized by diagnostic images of pancreatic enlargement and irregularly narrowed main pancreatic ducts. It is a condition that responds dramatically to corticosteroid therapy [ 6 – 8 ]. Corticosteroids are frequently used for the treatment of inflammatory conditions and autoimmune diseases, but are widely recognized to cause hyperglycemia and insulin resistance when used at high doses and for long durations [ 9 , 10 ].
Herein, we report the case of a patient in whom uncontrolled diabetes as a direct result of AIP and subsequent steroid treatment was successfully treated by the addition of empagliflozin to his insulin therapy. 2. Case Report
A 66-year-old Japanese man, 177 cm tall and weighing 66 kg (body mass index of 21.1), had been treated for hypertension for more than seven years. He had yearly medical evaluations but was never diagnosed with diabetes (postprandial glucose and hemoglobin A1c [HbA1c] levels in March 2017: 141 mg/dL and 5.4%, respectively). However, results of an annual medical check-up in March 2018 showed remarkable elevation of postprandial glucose and HbA1c levels (265 mg/dL and 11.4%, respectively). The following month (April), he reported symptoms of thirst and polyuria. His postprandial glucose and HbA1c levels on that day were 529 mg/dL and 13.1%, respectively. A high glycoalbumin level (43.2%) also suggested acute glucose elevation (Table 1 ). The patient’s anti-glutamic acid decarboxylase antibody test was negative; however, because his postprandial C-peptide level was low (1.15 ng/mL), the patient’s pancreas presumably had reduced insulin-secreting capacity. We noted that the patient’s daily life had not changed in years; and he had no diabetic complications such as retinopathy, nephropathy, or neuropathy. Table 1: Postprandial laboratory results on patient’s first visit.
To identify the cause of hyperglycemia, we performed several imaging studies. Abdominal computed tomography, magnetic resonance imaging, and magnetic resonance cholangiopancreatography (MRCP) revealed diffuse swelling that extended from the pancreatic body to tail (Figures 1(a) – 1(c) ). In addition, MRCP showed narrowing of the associated main pancreatic duct (Figure 1(c) ). The patient did not complain of any digestive symptoms such as upper abdominal pain; however, based on the imaging scans and elevation of serum immunoglobulin G4 (IgG4) levels (141.0 mg/dL), we diagnosed him with type 1 AIP. Figure 1: (a) An abdominal computed tomography scan performed on the patient’s first visit shows diffuse swelling extending from the pancreatic body to tail. The arrow indicates the affected portion of the pancreas. (b) Magnetic resonance image (T2 weighted image) of the abdomen prior to prednisolone therapy reveals diffuse swelling extending from the pancreatic body to tail. (c) MRCP prior to prednisolone therapy shows narrowing of the main pancreatic duct extending from the pancreatic body to tail.
To control diabetes, the patient began self-administering insulin injections: insulin aspart (Novo Nordisk) three times per day before each meal and insulin degludec (Novo Nordisk) before going to bed. Because tight adjustment of insulin dosage is required for achieving good glycemic control, the patient received a flash glucose monitoring system (Freestyle Libre™; Abbott Diabetes Care, Witney, UK) [ 11 ] upon initiation of insulin. He initially had considerable ketosis (Table 1 ), but, soon after, the levels of total ketone bodies, acetoacetate, and β -hydroxybutyrate declined to the normal range (36 μ mol/L, 12 μ mol/L, and 24 μ mol/L, respectively). By the end of April, the patient’s total insulin dosage was 36 units/day (Figure 2(a) ). In May, prednisolone (35 mg/day) was initiated for the treatment of AIP. At that time, 42 units/day of insulin was not sufficient to control glucose elevation (Figure 2(b) ); the patient required a maximum of 52 units/day (Figure 2(c) ). One month later, IgG4 levels declined to 54.3 mg/dL. The dosage of prednisolone, which was being tapered by 5 mg/day every 2 weeks, was 20~25 mg/day; and the total dosage of insulin was also lower than that of the previous month. However, 42 units/day of insulin was required to maintain glycemic control (Figure 2(d) ). In addition, the combination of high-dose insulin and prednisolone caused our patient to gain 3.6 kg weight from the start of prednisolone initiation. Figure 2: The results of continuous glucose monitoring (CGM) with the flash glucose monitoring system. Closed arrowheads indicate the timing of the patient’s meals and insulin injections. Open arrowheads indicate the timing of the patient’s insulin injections before sleep. Values adjacent to the arrowheads indicate the number of units of insulin injected. (a) One representative pattern of CGM prior to initiation of prednisolone. (b) Initiation of 35 mg/day of oral prednisolone. (c) Two days after initiation of prednisolone. Total dosage of insulin was increased to 52 units/day. (d) Because of the amelioration of AIP, prednisolone dosage was reduced to 25 mg/dL; however, 42 units/day of insulin was required to maintain glycemic control. (e) First day of empagliflozin administration. Hypoglycemia recorded at 5 AM to 6 AM and approximately 8 PM. (f) Twenty days after empagliflozin initiation. (g) CGM pattern of patient on empagliflozin only.
To improve glycemic control, empagliflozin was added to insulin therapy. Because we expected empagliflozin to lower blood glucose levels, we reduced the dosage of insulin to 29 units/day beforehand. Nevertheless, the patient experienced hypoglycemia 1 hour after breakfast and 1 hour after dinner on the day of empagliflozin initiation (Figure 2(e) ). By the end of June, 20 days after the addition of empagliflozin, the patient had lost 1.2 kg and his total insulin dosage had declined to 20 units/day (Figure 2(f) ). In July, the prednisolone dosage was reduced to 10 mg/day. Because the patient had achieved good glycemic control (postprandial glucose, HbA1c, and glycoalbumin levels: 159 mg/dL, 6.9%, and 14.3%, respectively), the total dosage of insulin was further reduced and then eventually discontinued (Figure 2(g) ). Thereafter, he maintained good glycemic control (postprandial glucose and HbA1c levels: 130–180mg/dL and 5.4–5.8%, respectively) despite receiving only empagliflozin for diabetes (Figure 3 ). However, his postprandial C-peptide level remained low (1.84 ng/mL), revealing that although the insulin-secreting capacity of his pancreas had slightly recovered, it remained insufficient. Figure 3: Changes in glycemic control and clinical course of AIP during prednisolone therapy. HbA1c levels (circles) and serum IgG4 levels (squares) declined over the course of treatment.
In October, the patient’s prednisolone dosage was 4 mg/day. His follow-up magnetic resonance imaging and MRCP showed that both the diffuse swelling of the pancreatic tail and narrowing of the associated main pancreatic duct had been ameliorated (Figures 4(a) and 4(b) ). To date, the patient’s AIP is well controlled and has not relapsed. Figure 4: (a) Magnetic resonance image (T2 weighted image) of the abdomen after prednisolone therapy reveals amelioration of the diffuse swelling that had affected the pancreas from body to tail. (b) MRCP after prednisolone therapy revealed amelioration of the narrowing of the main pancreatic duct. 3. Discussion
The international consensus diagnostic criteria for AIP identify two subtypes: type 1 is characterized by serum IgG4 elevation and the classic histopathological patterns of lymphoplasmacytic sclerosing pancreatitis; type 2 is characterized by idiopathic duct-centric pancreatitis and is not associated with IgG4 levels [ 12 – 14 ]. Although the clinical findings in AIP are nonspecific, the most common presentation is obstructive jaundice and upper abdominal pain [ 6 , 7 ]. Approximately 40–80% of patients with AIP reportedly also present with diabetes—some with simultaneous onset with AIP and some with exacerbation of preexisting diabetes [ 8 , 14 – 21 ]. In addition, some patients develop diabetes after the start of steroid therapy, the outcome of which varies with regard to glycemic control [ 17 , 18 , 20 , 22 – 24 ].
The diabetes associated with AIP is assumed to be caused by a reduction in insulin secretion. This may be the result of various mechanisms. For one, AIP is characterized by infiltration of cluster of differentiation (CD)8 and CD4 T lymphocytes, which surround ductal cells and secrete cytokines to suppress and destroy β -islet cells of the pancreas [ 22 , 23 ]. In addition, inflammation and fibrosis of exocrine glands is associated with the obstruction of blood flow in the endocrine glands, that results in ischemia of islet cells and dysfunctional insulin secretion. Furthermore, extensive destruction of the pancreatic islets caused by direct infiltration of inflammatory cells and fibroblasts proliferation also leads to dysfunctional insulin secretion [ 14 , 16 , 20 , 23 – 27 ].
Glucocorticoids are counterhormones against insulin [ 9 , 10 ], with mechanisms that include reduction of glucose uptake, induction of hepatic glucose production, and direct inhibition of insulin release [ 28 – 30 ]. Glucocorticoid-induced hyperglycemia is a common condition, which is often considered postprandial hyperglycemia [ 31 , 32 ]. Prominent hyperglycemia is most often observed when individuals with known diabetes take high doses of glucocorticoids, but may also occur with intake of moderate and low doses in individuals without a known risk [ 29 , 31 , 33 ]. The odds ratio for new-onset diabetes mellitus in patients treated with glucocorticoids ranges from approximately 1.5 to 2.5, and the total glucocorticoid dose and duration of therapy are strong predictors of diabetes induction [ 32 ].
Thus, initiation of steroid therapy in patients with AIP may induce the onset of diabetes or worsen glycemic control in those with preexisting diabetes [ 34 ]. However, steroid therapy also inactivates inflammatory cells and fibroblast function, and may improve insulin secretion by controlling a series of autoimmune mechanisms, including cytokine production [ 16 , 25 ]. It has been reported that pancreatic endocrine function improves after treatment with steroids in 25–45% of patients with AIP [ 20 , 24 , 35 ], with some patients eventually achieving a medication-free status [ 34 ]. Indeed, Miyamoto et al. reported that three months after the start of steroid therapy in patients with AIP and simultaneous onset of diabetes mellitus, 54% of patients experience improvement in diabetes, 36% do not have any change, and 9% have worsening of diabetes [ 16 ]. In addition, they noted that the long-term positive effect of corticosteroid therapy on glucose tolerance might be greater than its short-term negative effect on insulin [ 16 ].
Approximately half of patients with AIP-associated pancreatic diabetes are treated with insulin [ 35 ]. Such therapy is effective in lowering blood glucose. However, patients must be monitored for hypoglycemia and undesirable weight gain, especially when insulin dosage is increased. SGLT2 inhibitors may have glycemic benefits in patients with type 1 or type 2 diabetes who are on insulin therapy [ 36 ]. Accumulating reports indicate that SGLT2 inhibitors are well tolerated, and their addition to insulin therapy improves glycemic control and reduces body weight such that insulin dosages could sometimes be reduced [ 37 – 52 ]. The mechanism was explained by Ferrannini et al., who reported that empagliflozin lowers fasting and postprandial glycemia by inducing glycosuria, which improves β cell function and insulin sensitivity in patients with type 2 diabetes [ 53 ]. This was noted despite the fall in insulin secretion and tissue glucose disposal, and the rise in endogenous glucose production that occurs after a single dose of 25 mg empagliflozin [ 53 ]. We were able to reduce our patient’s total insulin dosage upon initiation of empagliflozin. This lowered his risk of hypoglycemia and suppressed weight gain. Although improvement in glycemic control and reduction in total insulin dosage could have been the result of AIP amelioration alone, we believe that empagliflozin accelerated improvement of glycemic control in our patient.
One of the risks of SGLT2 inhibitors is diabetic ketoacidosis (DKA) [ 4 , 5 ]. Similar to classic DKA, ketone accumulation in SGLT2 inhibitor-associated DKA is downstream of insulin deficiency and glucagon elevation, promoting lipolysis and hepatic ketogenesis. SGLT2 inhibitor-enhanced glucosuria effectively lowers plasma glucose levels, which decreases insulin secretion from pancreatic β cells. SGLT2 inhibitor-mediated glucosuria and attenuation of sodium reabsorption in the kidneys may also indirectly expand the ketone reservoir by enhancing renal ketone reabsorption [ 54 – 56 ]. Although our patient initially had prominent ketosis, the ketosis improved soon after initiation of insulin therapy. Although we rechecked for ketosis throughout his treatment with empagliflozin, no further signs of ketosis were detected.
In conclusion, this case report suggests that the combination of insulin and SGLT2 inhibitor can be effective for the treatment of secondary diabetes, such as prednisolone-induced diabetes associated with the treatment of AIP in our patient. Further studies on a larger scale are required to confirm the effectiveness of this combination for the treatment of diabetes in patients on corticosteroid therapy. Ethical Approval
All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and the Helsinki Declaration of 1975, as revised in 2000 and 2008. In addition, this case report was approved by the Ethics Committee of Sanno Hospital. Consent
The authors obtained written informed consent from the patient for publication. Conflicts of Interest
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Yes, 10mg weekly taper does sound fast.
Last year, I dealt with a year long flare where I was originally on pentasa, and it eventually became ineffective for me. So, I had a colonoscopy , and my doctor decided to put me on 40mg prednisone to calm down the flare and 50mg 6mp for maintenance. My symptoms went away, tapered off the prednisone, and my symptoms reappeared about a week after fully tapering. (I tapered 5mg weekly) So my doctor put me back on the prednisone, and the same thing happened again.
We finally decided the 6mp was not doing anything for me, so I started Remicade , and that was what finally put me back in remission. I think what I am trying to say is if you try tapering several times and your symptoms reappear, it is a sign that you need to switch to a different maintenance medication.

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Are you on any maintenance medication? If you are not on a maintenance medication and try tapering from prednisone , you are very likely to flare again.

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