scholarly journals Muscle Infarction Following Rapid Glycemic Control in a Patient With Diabetes-Associated Microvascular Disease

Cureus ◽  
2021 ◽  
Author(s):  
Leonor Boavida ◽  
Joana Carvalho ◽  
Susana Oliveira ◽  
José Delgado Alves
2020 ◽  
Vol 8 (2) ◽  
pp. 340-343
Author(s):  
Khaled Ali ALawaini ◽  
Hanen Daw Sweed ◽  
Khalod Mohamed Sawesi ◽  
Fatma Abdusalam Kamoka ◽  
Sara Abugalel Alakrme ◽  
...  

Background: Diabetes is a public health challenge facing the world. Awareness and long term diabetes have an enormous effect, including cardiovascular disease and microvascular disease. Objective: This study aimed to estimate diabetes incidence and it is complications. Methods: A hundred diabetic patients who attended Galil diabetic center in Sabratha city had participated in this study in May 2013. Results: The mean age was 56 years old. Diabetes was more prevalent in females than in males (62%vs38%). The mean blood glucose concentration was 168 mg/dl, reflecting poor glycemic control, as 16% of diabetic patients moved to treatment with insulin. Conclusion: Poor glycemic control means of fasting plasma glucose was 168 mg/dl, and 16% started to use insulin therapy, along with 15% had hypertension.


2011 ◽  
Vol 14 (1) ◽  
pp. 79-88 ◽  
Author(s):  
Toni Terry ◽  
Kalyani Raravikar ◽  
Nalurporn Chokrungvaranon ◽  
Peter D. Reaven

2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Sisira Sran ◽  
Manpreet Sran ◽  
Nicole Ferguson ◽  
Prachi Anand

We report a case of sudden thigh pain from spontaneous quadriceps necrosis, also known as diabetic myonecrosis, in a 28-year-old patient with poorly controlled diabetes mellitus. Diabetic muscle infarction is a rare end-organ complication seen in patients with poor glycemic control and advanced chronic microvascular complications. Proposed mechanisms involve atherosclerotic microvascular occlusion, ischemia-reperfusion related injury, vasculitis with microthrombi formation, and an acquired antiphospholipid syndrome. Diabetic myonecrosis most commonly presents as sudden thigh pain with swelling and should be considered in any patient who has poorly controlled diabetes mellitus.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A377-A377
Author(s):  
Timothy Reisner ◽  
James K Burks

Abstract Background: Diabetic myonecrosis is a rare complication of diabetes mellitus with less than 200 cases reported in the literature since initial description in 19651. Diabetic myonecrosis most commonly affects the thigh and usually presents with acute muscle pain, edema, and erythema in the absence of trauma or fever1. The pathogenesis has yet to be elucidated—atherosclerosis, microangiopathy, vasculitis, and ischemia-reperfusion injury have been theorized. Laboratory findings are relatively nonspecific—of the findings reported in a systematic review, CRP was elevated in 90%, ESR elevated in 83.3%, WBC elevated in 42.5%, and CK elevated in 31.6%1. Definitive diagnosis can be made by muscle biopsy which demonstrates muscle necrosis and edema; however, it is not routinely recommended due to procedural complications. MRI is the diagnostic modality of choice for diabetic myonecrosis which is both sensitive and specific for the diagnosis2. Clinical Case: 76-year-old male with T2DM presented to regional hospital with severe right lower leg pain in the absence of fever, tachycardia, hypotension, or recent trauma. Physical exam demonstrated discrete erythema of distal 2/3 of posterior right lower leg extending to the ankle distally. Labs demonstrated normal CK, elevated ESR, HgbA1c 8.2%, and negative blood cultures. MRI of the right lower extremity demonstrated abnormal prolongation of T2 relaxation time involving posterior muscle compartment including soleus and gastrocnemius with associated perifacial and subcutaneous edema. These findings were consistent with diabetic myonecrosis without evidence of osteomyelitis or abscess. Rest, optimal glycemic control, and aspirin were recommended and patient improved gradually with complete clinical resolution on outpatient follow-up. Conclusions: Diabetic myonecrosis is a rare complication of diabetes and should be considered in patients presenting with acute muscle pain. Among cases described in literature, 5.7% have affected the soleus and 5% have affected the gastrocnemius respectively1. The diagnostic modality of choice is contrast enhanced MRI with typical findings including hyperintense signal on T2 weighted images with associated muscular, perifascial, and/or subcutaneous edema3. The optimal treatment is yet unknown, but reasonable strategies based on case series include rest, glycemic control, and NSAID therapy1. References: 1. Horton WB, Taylor JS, Ragland TJ, Subauste AR. Diabetic muscle infarction: a systematic review. BMJ Open Diabetes Res Care. 2015;3(1):e000082. doi:10.1136/bmjdrc-2015-000082 2. Morcuende JA, Dobbs MB, Crawford H, Buckwalter JA. Diabetic muscle infarction. Iowa Orthop J. 2000;20:65–74. 3. Goswami P, Baruah MP. The Role of MRI in Diagnosis of Diabetic Muscle Infarction : an Underdiagnosed Entity. Int J Endocrinol Metab. 2012;9(2):353–355. doi:10.5812/kowsar.1726913X.1886


2008 ◽  
Vol 52 (2) ◽  
pp. 387-397 ◽  
Author(s):  
Bernardo Léo Wajchenberg ◽  
Nelson Rassi ◽  
Alina Coutinho R. Feitosa ◽  
Antonio Carlos Lerário ◽  
Roberto Tadeu Barcelos Betti

The association between type 1 diabetes and coronary heart disease has become very clear since the late 1970. It has been demonstrated that there is an important increased risk in morbidity and mortality caused by coronary artery disease in young adults with type 1 diabetes compared with the non diabetic population. The underlying pathogeneses is still poorly understood. While the role of glycemic control in the development of microvascular disease complication is well established its role in CVD in patients with DM1 remains unclear with epidemiologic studies reporting conflicting data. Recent findings from the DCCT/EDIC showed that prior intensive diabetes treatment during the DCCT was associated with less atherosclerosis, largely because of reduced level of HbA1c during the DCCT. The improvement of glycemic control itself appeared to be particularly effective in younger patients with shorter duration of the disease. Other analyses suggested the glycemia may have a stronger effect on CAD in patients without than in those with albuminúria. Other major determinants of coronary artery disease are the components of metabolic syndrome and the surrogate measure of insulin resistence: eGDR. It is proposed that patients with DM1 should have aggressive medical therapy, risk factor modification and careful monitoring not only of his blood sugar but also of the other processes involved in the atherosclerotic process, mostly the ones with family history of type 2 diabetes.


Metabolism ◽  
2000 ◽  
Vol 49 (1) ◽  
pp. 88-91 ◽  
Author(s):  
Bijan Roshan ◽  
Geoffrey H. Tofler ◽  
Larry A. Weinrauch ◽  
Ray E. Gleason ◽  
Joanne A. Keough ◽  
...  

2020 ◽  
Vol 21 (4) ◽  
pp. 613-629 ◽  
Author(s):  
Jacob Bar-Tana

Abstract The current paradigm of type 2 diabetes (T2D) is gluco-centric, being exclusively categorized by glycemic characteristics. The gluco-centric paradigm views hyperglycemia as the primary target, being driven by resistance to insulin combined with progressive beta cells failure, and considers glycemic control its ultimate treatment goal. Most importantly, the gluco-centric paradigm considers the non-glycemic diseases associated with T2D, e.g., obesity, dyslipidemia, hypertension, macrovascular disease, microvascular disease and fatty liver as ‘risk factors’ and/or ‘outcomes’ and/or ‘comorbidities’, rather than primary inherent disease aspects of T2D. That is in spite of their high prevalence (60–90%) and major role in profiling T2D morbidity and mortality. Moreover, the gluco-centric paradigm fails to realize that the non-glycemic diseases of T2D are driven by insulin and, except for glycemic control, response to insulin in T2D is essentially the rule rather than the exception. Failure of the gluco-centric paradigm to offer an exhaustive unifying view of the glycemic and non-glycemic diseases of T2D may have contributed to T2D being still an unmet need. An mTORC1-centric paradigm maintains that hyperactive mTORC1 drives the glycemic and non-glycemic disease aspects of T2D. Hyperactive mTORC1 is proposed to act as double-edged agent, namely, to interfere with glycemic control by disrupting the insulin receptor-Akt transduction pathway, while concomitantly driving the non-glycemic diseases of T2D. The mTORC1-centric paradigm may offer a novel perspective for T2D in terms of pathogenesis, clinical focus and treatment strategy.


2001 ◽  
Vol 120 (5) ◽  
pp. A232-A232
Author(s):  
J HAMMER ◽  
S HOWELL ◽  
M HOROWITZ ◽  
N TALLEY

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