Pathophysiology, prevention, and treatment of beriberi after gastric surgery.

Beriberi is a nutritional complication of gastric surgery, caused by deficiency of vitamin B1, or thiamine. Thiamine deficiency leads to impaired glucose metabolism, decreased delivery of oxygen by red blood cells, cardiac dysfunction, failure of neurotransmission, and neuronal death. This review describes the history and pathophysiology of beriberi as well as the relationship between beriberi and nutritional deficiencies after gastric surgery. A literature review of the history and pathophysiology of beriberi and the risk factors for thiamine deficiency, particularly after gastric resection or bariatric surgery, was performed. Recommendations for nutritional follow-up post gastric surgery are based on current national guidelines. Patients may have subclinical thiamine deficiency after upper gastrointestinal surgery, and thus beriberi may be precipitated by acute illness such as sepsis or poor dietary intake. This may occur very soon or many years after gastrectomy or bariatric surgery, even in apparently well-nourished patients. Prompt recognition and administration of supplemental thiamine can decrease morbidity and mortality in patients with beriberi. Dietary education post surgery and long-term follow-up to determine nutritional status, including vitamin and mineral assessment, is recommended for patients who undergo gastric surgery.

Case report: pericardial effusion with constrictive physiology in a patient with wet beriberi.

Wet beriberi-induced pericardial effusion has rarely been previously described. Little is known about the effect of beriberi-induced pericardial effusion on hemodynamics. Here we present a case of wet beriberi with pericardial effusion that exhibited constrictive physiology, which was dramatically improved after treatment. A 61-year-old male patient was admitted to our hospital for progressive leg edema, dyspnea on exertion, and lower-extremity muscle weakness. Echocardiography showed a hyperkinetic left ventricle and a moderate amount of pericardial effusion. Hemodynamic measurements, including simultaneous measurement of left and right ventricular pressures, revealed high output heart failure and constrictive physiology. Blood test showed lactic acidosis, and low level of serum thiamine levels; consistent with a diagnosis of wet beriberi. After thiamine replacement therapy, the patient's hemodynamic state rapidly improved. Additionally, pericardial effusion decreased and constrictive physiology was successfully resolved. No other possible causes of pericardial effusion could be identified, with the exception of thiamine deficiency. This case illustrates the importance of considering wet beriberi as a possible cause of pericardial effusion with constrictive physiology.

Elevated Lactate Secondary to Gastrointestinal Beriberi.

Thiamine deficiency usually occurs with prolonged nutritional deficiency and is almost universally identified with Wernicke's encephalopathy or beriberi. It is also, however, a rare cause of elevated lactate and gastroenterological symptoms. This case report describes a 30-year-old man with 2 weeks of gastroenterological symptoms and intermittent oral intake, who was found to have an elevated lactate level. Neurological exam was normal and an extensive workup was negative, but after being treated with thiamine, his lactate level improved overnight and all of his symptoms resolved. Thiamine levels returned low at 44 nmol/L (normal 78-185 nmol/L). Lack of recognition of this phenomenon, while rare, can lead to unnecessary tests and procedures and increased morbidity and mortality.

Shoshin Beriberi in Critically-Ill patients: case series.

Thiamine plays a fundamental role in cellular metabolism. The classical syndrome caused by thiamine deficiency is beriberi, and its fulminant variant, once considered an uncommon finding, is now encountered among the critically ill.We present a case series of four critically ill non-septic non-alcoholic patients with severe lactic acidosis and refractory cardio-circulatory collapse caused by acute fulminant beriberi, which drastically responded to thiamine administration.In critical care settings, increased awareness of this life-threatening but reversible condition is a requirement, especially among patients receiving parenteral nutrition and those with unexplained recalcitrant lactic acidosis.

Thiamine deficiency and cardiac dysfunction in Cambodian infants.

OBJECTIVES: To compare blood thiamine concentrations, echocardiography findings, and plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels in infants with clinically diagnosed beriberi and healthy matched controls, and to evaluate changes after thiamine treatment. STUDY DESIGN: Sixty-two Cambodian infants (20 cases and 42 controls), aged 2-47 weeks, were enrolled in this prospective study. Echocardiography and phlebotomy were performed at baseline and after thiamine treatment. RESULTS: Both cases and controls were thiamine-deficient, with median blood thiamine diphosphate (TDP) concentrations of 47.6 and 55.1 nmol/L, respectively (P = .23). All subjects had normal left ventricular ejection fraction. The median NT-proBNP concentration in cases (340 pg/mL [40.1 pmol/L]) was higher than previously reported normal ranges, but not statistically significantly different from that in controls (175 pg/mL [20.7 pmol/L]) (P = .10), and was not correlated with TDP concentration (P = .13). Two cases with the lowest baseline TDP concentrations (24 and 21 nmol/L) had right ventricular enlargement and elevated NT-proBNP levels that improved dramatically by 48 hours after thiamine administration. CONCLUSION: Only a minority of thiamine-deficient Cambodian infants demonstrate abnormal echocardiography findings. Thiamine deficiency produces echocardiographic evidence of right ventricular dysfunction, but this evidence is not apparent until deficiency is severe. NT-proBNP concentrations are mildly elevated in sick infants with normal echocardiography findings, indicating possible physiological changes not yet associated with echocardiographic abnormalities.

Increase of serum vascular endothelial growth factors in wet beriberi: two case reports.

Beriberi is a disease caused by thiamine deficiency resulting in peripheral neuropathy and myocardial dysfunction. Increases in vascular endothelial growth factor (VEGF) are seen in polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes, called POEMS syndrome. We present herein two cases of wet beriberi accompanied by a moderate increase in VEGF level. Serum VEGF decreased after treatment in both cases. Our experience with these cases suggests that beriberi should be considered in the differential diagnosis of polyneuropathy with a moderate increase in serum VEGF, and that the serum VEGF level may be a therapeutic marker for beriberi.

Outbreak of beriberi in the state of Maranhão, Brazil: revisiting the mycotoxin aetiologic hypothesis.

Beriberi is caused by thiamine deficiency. Early 20th century epidemics in Japan were attributed to rice contaminated by citreoviridin mycotoxin. Our investigation of an outbreak of beriberi in Brazil showed an association of beriberi with the consumption of poor quality subsistence farming rice, although, unlike other investigators of this outbreak, we did not identify citreoviridin producing fungi in the implicated rice.

Lactate in a laubenpieper.

Acid-base disorders seldom kill; however, the mechanisms and associated complications certainly do. We recently encountered a patient with a mysterious lactic acidosis. The patient proved to be a most capable teacher of important lessons.

Outbreak of beri-beri in The Gambia.

In 1988, an outbreak of beri-beri occurred in The Gambia during the rainy season. At least 140 people were affected, and 22 died. A clear response to thiamine was observed in 8 patients who were in hospital, and the outbreak resolved after distribution of thiamine in the community. Gradual replacement of traditional cereals with imported milled rice may have increased susceptibility to beri-beri.

PIP: This study examined an outbreak of beri-beri which occurred in The Gambia between July and September 1988. 140 people were affected and 22 died. The outbreak resolved after distribution of thiamine in the community. Gradual replacement of traditional cereals with imported milled rice may have increased susceptibility to beri-beri. The 1st reports of beri-beri came from the village of Chilla where 25 of 975 inhabitants described their symptoms. Active case-finding located 38 affected people. All patients had peripheral edema and 1/3 had a mixed motor and sensory neuropathy. The earliest symptoms started 3 weeks after the start of the rainy season. All inhabitants were Muslim whose staple diet is millet and imported rice from Thailand. Attack rates in Chilla and in other clinics were highest in young men. Within a few days of hospitalization (8) all patients responded rapidly to treatment of oral thiamine of 10 mg/day. Since 22 people with symptoms suggestive of beri-beri had already died in the outbreak area before thiamine became available the authors chose not to assign patients to treatment and non-treatment groups. As a result of the response to treatment of the hospital patients, thiamine was distributed to health centers and village health workers in the affected areas. Daily thiamine (200 mg) was given until symptoms were resolved. The trend towards consumption of imported rice and away from other cereals has gradually reduced people's thiamine intake and thiamine stores. In the affected area, this factor, combined with the high rainfall, high agricultural workload, cooking methods, and possible thiamine antagonists, led to the outbreak.

The role of selenium deficiency in occidental dilated cardiomyopathy.

The whole blood selenium concentrations were measured in 14 consecutive cases of catheter-proven dilated cardiomyopathy. The mean range of selenium was 59 ng/mL (SD 14). Patients with coronary heart disease had a mean value of 44 ng/mL (9.7) and normal controls had 78 ng/mL (20.1). These results would not support the hypothesis that selenium deficiency is an important causative agent in dilated cardiomyopathy in New Zealand.

The haemodynamic, histopathological and hormonal features of alcoholic cardiac beriberi.

Five cases of cardiac beriberi occurring in chronic alcoholics are described. The clinical diagnosis was based on the presence of biventricular failure, low dietary intake of thiamine and the therapeutic response to oral thiamine. Complicating cardiac disease was excluded by haemodynamic studies, left ventriculography; coronary angiography and endomyocardial biopsy. Haemodynamic measurements including quantitative left ventriculography are reported. They indicate that left ventricular function is depressed despite elevated cardiac output. Biopsy material was studied by light and electron microscopy. No lesion specific to beriberi was detected by either technique although the biopsies were quantitatively abnormal. The histological changes resemble those in early reports based on necropsy material, and consist of vacuolation and intercellular oedema in the early stages with myofibre hypertrophy, fibrosis and cellular infiltration in the chronic cases. The transketolase test and response to intravenous thiamine during catheter studies are valuable diagnostic tests. Plasma renin, angiotensin II and aldosterone levels were lower than in patients with low output heart failure. The incidence of cardiac beriberi appears to be greater than is generally realized.

Blood vitamin B1, transketolase and thiamine pyrophosphate (TPP) effect in beriberi patients, with studies employing discriminant analysis.

In recent years, many cases of beriberi have been reported throughout Japan. One may assume that a great many healthy subjects suffer from a subclinical thiamine deficiency. The present study was carried out in order to examine thiamine status in 21 beriberi patients and 674 apparently normal subjects. In the beriberi patients the total vitamin B1 in whole blood and transketolase activity in the hemolysate were significantly lower, and the thiamine pyrophosphate effect was significantly higher, compared to normal subjects. However, these two groups could not be clearly separated by these biochemical parameters because of significant overlap. On analyzing the results of these biochemical parameters by discriminant analysis, beriberi could be diagnosed with an accuracy of 87,7%. Thus, vitamin B1 levels in blood, transketolase activity and the thiamine pyrophosphate effect in the hemolysate are useful biochemical indices for the diagnosis of beriberi. Above all, the thiamine pyrophosphate effect proved to be the most effective parameter in distinguishing the beriberi group from normal subjects.

Two cases of shoshin beri beri with hemodynamic and plasma catecholamine data.

Two fulminant forms of beri beri ("shoshin beri beri") have been the subject of detailed study; circulating catecholamines reached very high levels. The evolution of hemodynamic parameters after treatment with thiamin is described. One case died and the histological lesions corresponded to those of "chronic congestive beri beri".