Diabetic Diarrhea

Ogbonnaya, Kalu I.

doi:10.1001/archinte.1990.00390140018005

Cited by 57 publications

(9 citation statements)

References 3 publications

(3 reference statements)

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“…[15][16][17][18][19][20][21][22][23][24][25][26] Other contributing factors include high oxalate diet, excessive vitamin C intake, diabetic gastroenteropathy, inadequate calcium supplementation, and hyperparathyroidism. [15,[27][28][29][30][31][32][33] Increased enteric oxalate absorption that results from intraluminal free fatty acid and calcium binding due to fat malab-sorption can lead to hyperoxaluria and increased urine calcium oxalate supersaturation. [16] Aside from dietary source, oxalate that has accumulated due to decreased renal excretion among patients with kidney disease lead to hyperoxaluria after renal transplant.…”

Section: Discussionmentioning

confidence: 99%

Gastric bypass oxalosis in renal transplant: clinicopathologic correlates

Salazar

Taber

O'Neill

et al. 2016

CRCP

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Background: Reports of oxalate nephropathy after gastric bypass (GB) leading to graft loss of kidneys causes concern for transplant professionals. We examined the clinical phenotype of GB related oxalate nephropathy (ON), its contribution to graft loss and propose a management strategy to mitigate graft loss in renal transplant recipients. Methods: Retrospective case series of patients who had GB surgery prior to renal transplant at a single institution were studied. Oxalate burden in renal transplant biopsies was quantified by intratubular calcium/glomeruli (Ca T/G) ratio and correlated with other clinical covariates. Results: We identified 16 GB patients; the mean BMI pre-GB was 52.5 kg/m 2 (range 42-80), with a follow-up BMI of 30.9 kg/m 2 (range 22-36.5) at transplant evaluation. Among 11 patients who had for cause biopsies, 3 patients had significant intra tubular allograft calcium oxalate deposition with a median time from graft to failure of 9 months. Among patients with functioning grafts, follow up creatinine averaged 1.6 mg/dl (0.9-3.4 mg/dl); median follow up was 4 years (0.5-7 years). Conclusions: The relationship between GB and ON post renal transplant is variable. The expression of ON after acute kidney injury (AKI) suggests that mitigating strategies should be directed at preventing alloimmune and other forms of AKI in addition to managing oxalate intake.

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Section: Discussionmentioning

confidence: 99%

Gastric bypass oxalosis in renal transplant: clinicopathologic correlates

Salazar

Taber

O'Neill

et al. 2016

CRCP

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“…It seems to be more common in middle-aged diabetic patients who are insulin dependent and have long-standing poorly controlled diabetes [33]. The causes are usually multifactorial and include neuropathic motility disturbances and bacterial overgrowth, pancreatic exocrine insufficiency, electrolyte imbalances, and altered gut hormone production [34]. Several motility abnormalities have been described in the stomach and small intestine of diabetic patients.…”

Section: Diarrheamentioning

confidence: 99%

“…The diarrhea is characterized by intermittent brown watery, voluminous stools and is occasionally accompanied by tenesmus. It can occur at any time of the day but is often nocturnal [34]. Surprisingly, patients do not have weight loss, cachexia, or other biochemical abnormalities observed in malabsorptive disorders.…”

Section: Diarrheamentioning

confidence: 99%

Gastrointestinal disturbances in diabetes

Chandran¹,

Chu²,

Edelman³

2003

Curr Diab Rep

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Gastrointestinal disorders are common in patients with diabetes mellitus. As many as 75% of patients visiting diabetes clinics will report significant gastrointestinal (GI) symptoms. The symptom complex experienced may vary widely. Many patients go undiagnosed and undertreated. Patients with a history of retinopathy, nephropathy, or neuropathy should be presumed to have GI abnormalities until proven otherwise. The workup should start with a thorough patient history and appropriate laboratory, radiographic, and GI testing. In addition to pharmacologic therapy, glycemic control and dietary manipulation play an important role in managing GI disorders in people with diabetes.

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“…Diabetic diarrhoea is a chronic condition predominantly affecting middle‐aged patients with poorly controlled type 1 diabetes 1 . It has a male to female ratio of 3 : 2 2 . The overall incidence is as high as 10−22%, 3 although much of this is very mild, with severe cases such as those reported being rare.…”

mentioning

confidence: 99%

“…Other mechanisms, which may contribute to the diarrhoea, are bacterial overgrowth, bile salt malabsorption, pancreatic insufficiency and abnormalities in gut hormone production 2 . These proposed mechanisms have led to first line treatments for diabetic diarrhoea of broad‐spectrum antibiotics 1 including erythromycin (which interacts with motilin receptors), cholestyramine 2 and pancreatic enzyme supplements. Commonly used antidiarrhoeal agents such as codeine, loperamide and atropine may decrease stool number, but often do not reduce stool volume 2 …”

mentioning

confidence: 99%