Distinct forms of diabetes have been noted in its more atypical presentations and forms. Tropical Diabetes is one of them, and it was classified as such long ago based on patients’ clinical data in their history of travel to subtropical areas. In simpler terms, the type of diabetes which derives from tropic and subtropic regions is described as Tropical Diabetes. This subtype was initially postulated to be prevalent in underdeveloped nations suffering from chronic shortage of food and malnutrition. It consists of an array of varieties which include Fibrocalculous Pancreatic Diabetes (FCPD) and Malnutrition-Related Diabetes Mellitus MRDM. Alongside this initial definition, modern findings on tropical diabetes surfaced. A wider range of consequences including genetic factors and dietary toxins like cyanogenic glycosides from cassava and other regions into the picture. In addition, the epidemiological transition pertaining to newly developed and moderately developed tropical countries has further changed the scope of this classification. Such countries are undergoing progression within urban centers, encountering shifts with their diets, and the burden concerning metabolic diseases. Along these factors, all these transcend the known limits of tropical diabetes.

This review explains the development of tropical diabetes from a historical, pathophysiological, clinical, and epidemiological perspective, with a focus on the crossroad of exocrine pancreatic insufficiency, insulin deficiency, and some degree of insulin resistance in the studied population, new data on SPINK1 mutations and other genetic markers of the disease are also provided. Distinction of diabetes from other types is supported by its unique features like not having ketosis with the variable insulin therapy response set it apart from classical type 1 and 2 diabetes. Moreover, the review evaluates the tropical diabetes and micronutrient deficiency relationship, in particular with vitamin A suspected to play a role in pancreatic β-cell dysfunction. Examining the context of tropical diabetes also implies diagnostic and therapeutic challenges as well as reclassification possibilities. Conclusions reflect the importance of diagnostics tailored to the heterogeneity of the diabetic phenotypes in these regions. Thus, the goal of the review is situated within what tropical diabetes is and how it can be clinically identified and managed in endemic areas integrating historical paradigms with modern progress.

Keywords: Tropical diabetes, fibrocalculous pancreatic diabetes (FCPD), malnutrition-related diabetes mellitus (MRDM), ketosis-resistant diabetes, pancreatic calcification, dietary cyanide, SPINK1 mutation, exocrine pancreatic dysfunction, insulin deficiency, precision medicine, metabolic transition.

Diabetes is a disease threatening global health and one suffering significantly in low and middle income countries. It is well known that type 1 and type 2 dominate the majority of attention, but there exists a lesser known variety from the tropics, and is historically known as tropical diabetes. After malnutrition related diabetes mellitus (MRDM) was first diagnosed, it was later refined into two sub-divisions, fibrocalculous pancreatic diabetes (FCPD) and protein-deficient pancreatic diabetes (PDPD) which both share traits of severe diabetes that is insulin deficient, along with severe and early onset of ketosis. Despite classification into subtypes, there is significant overlap within the clinical presentation of these conditions.

As with every other diabetes, tropical diabetes also shares the common quintessential feature of being associated with some form of exocrine pancreatic damage. This particular type differs from the more widely known classical type 1 diabetes, where autoimmune destruction of β-cells is the predominant mechanism. Not only is tropical diabetes known for having pancreatic exocrine dysfunction, but it also suffers from severe insulin resistance.

The chronic inflammation to the pancreas is usually related to dietary poisons like cyanogenic glycosides through the consumption of cassava, recurrent pancreatitis, and poor nutrition, especially lack of vitamin A. Certain recent studies on genetics have also found some mutations of the SPINK1 (serine protease inhibitor, Kazal type 1) gene which seem to lead towards fibrocalculous pancreatic diabetes towards gain of function diabetes. This has contributed more evidence to support the claim of a multi causative genetic environment interaction of the disease’s pathogenesis.  In terms of the epidemiology, within the last few years the South Asia, some regions of sub-Saharan Africa, and parts of Latin America Tropics have been diabetes positive where malnourishment and a specific diet has tended to dominate the paradigm of disease risk. However, as socio economic urbanization intensifies along with diet westernization the patterns of diabetes in tropical countries is starting to change highlighting the need for a shift in the classification and diagnosis of the disease. There is a rapid blurring of the border between tropical diabetes and the rest, which poses the question of whether tropical diabetes is an independent entity or part of a continuum. Tropical diabetes is one disease which is well spaced in the domain of endocrine global problem; however, it remains less studied due to misplacing it based on the challenges of diagnosis with the emerging geographical patterns of epidemiology. This Rodrigues explains the often poorly defined boundaries of this disease, particularly with its so-called ketosis-resistant diabetes which eases diagnosis as type 2 diabetes.

Metrics associated with clinical symptoms and treatment outcomes respond differently. Therefore, to maximize therapy effectiveness, it is important to utilize precision medicine strategies which are designed for metabolic and genetic system of the patients.  \\  \\  Tropical diabetes is a specific condition that warrants attention as it comes with its own set of challenges in terms of diagnosis, treatment, and epidemiology. This review combines historical aspects and new research data to create a comprehensive framework that improves diagnosis and treatment of tropical diabetes, hence, improving the health status of the population in the affected areas.

Types of tropical diabetes

Tropical diabetes is a blend of diabetes mellitus subtypes that primarily impacts people living in tropical and subtropical regions. It differs from the classical type 1 and type 2 diabetes due to its unique disease mechanisms, lesional forms, and causative factors. The most important categories include Malnutrition-Related Diabetes Mellitus (MRDM), Fibrocalculous Pancreatic Diabetes (FCPD), and Ketosis-Prone Diabetes (KPD). These forms differ in the degree of metabolic disturbances, damage to the pancreas, and their reaction to treatment.

Malnutrition-related diabetes mellitus (MRDM)

Definition

MRDM is a form of diabetes secondary to chronic protein energy malnutrition. It used to be observed in tropical malnourished populations where early life nutritional deprivation leads to long-term metabolic and pancreatic dysfunction.^7,9

Characteristics

MRDM is usually characterized by:

1. Occurring in adolescents or young adults, more commonly in patients with a past history of chronic malnutrition.
2. Severe insulinopenia as a result of incompetent pancreas function leading to insulin addiction, but insulin deficient state admits to no ketosis.⁷
3. Exocrine pancreatic insufficiency, usually accompanied by steatorrhea due to pancreatic insufficiency.⁹
4. Greater frequency in people living in poverty in tropical countries where undernutrition is chronic.¹¹

Subtypes of MRDM

Protein deficient pancreatic diabetes (PDPD)

1. Associated with long-standing protein and energy malnutrition resulting in atrophy of the exocrine pancreas.
2. Patients show marked deficiency of insulin and need to be placed on exogenous insulin treatment.⁹
3. Generally noted in people with lower body protein levels, especially in South Asia and regions of Sub-Saharan Africa.⁷

Fibrocalculous pancreatic diabetes (FCPD)

1. These are the complications and considerations of chronic calcific pancreatitis where there is extensive pancreatic fibrosis along with progressive failure of the β cells.
2. In contrast to PDPD, the evidence of pancreatic pathology is usually appreciated in the abdomen scans. There are confirmed cases of pancreatic calcifications.⁸
3. There is marked insulin deficiency, but patients are not likely to develop ketoacidosis, differentiating it from classic type 1 diabetes.⁹

Fibrocalculous Pancreatic Diabetes (FCPD)

Definition

FCPD is known as one of the most tropical diabetes where the causes include chronic calcific non-alcoholic pancreatitis. Leading to progressive exocrine followed by endocrine dysfunction of the pancreas. This form of diabetes has been well recognized and documented by WHO as a MRDM⁹ subtype disease.

Clinical Features

1. Weight Range: Generally between 40 kg for females and 50 kg for males. And the average age for presentation is 23 years.
2. Steatorrhea & Malabsorption: Due to exocrine pancreatic insufficiency leading to chronic diarrhoea and loss of weight.⁷
3. Insulin deficiency: Management is by using insulin but the patient is not able to undergo ketosis which is different from type 1 diabetes.⁹
4. Pancreatic Calcification: The most important feature of diagnosis of Fibrocalculous Pancreatic Diabetes, features of which are seen on plain abdominal X-ray and followed by ultrasound scan.⁸

FCPD is prevalent throughout tropical and subtropical regions such India, Bangladesh, some parts of Africa, and the Caribbean. In India, the disorder is commonly noted among low socioeconomic groups with history of sustained exposure to cassava and other cyanogenic diets which are believed to cause pancreatic damage.⁷

Ketosis-prone diabetes (KPD)

Definition

KPD is an uncommonly aggressive type of diabetes marked by episodic diabetic ketoacidosis (DKA) without any enduring need of exogenous insulin. It is both a type 1 and type 2 diabetes but does not have autoimmune features which makes it different from classical autoimmune diabetes.⁷

Characteristics

1. Intermittent Insulin Requirement: Unlike typical type 1 diabetes which is everlastingly dependent on insulin, KPD patients are able to recover some β-cell function and can stop insulin.⁸
2. Variable Insulin Deficiency: Some patients show somewhat preserved pancreatic function after a DKA episode.⁹
3. Absence of Autoimmunity: Unlike type 1 diabetes, KPD is devoid of islet-cell autoantibodies (GAD, IA-2, ZnT8.⁸
4. Strong Ethnic Predisposition: More common in African, Latino, and South Asian descent, especially those living in warm and moist parts of the world.¹¹

Pathophysiology

KPD is a range of metabolic dysfunction characterized by interspersed periods of β-cell decompensation and recovery. Some patients demonstrate reversible insulinopenia while others advance to be permanently insulin dependent (Table 1,2).⁸

Clinical in regard to complications of tropical diabetes

The term “tropical diabetes” encompasses three different sub-types of diabetes, which are: Malnutrition related diabetes mellitus (MRDM), Fibrocalculous pancreatic diabetes (FCPD), Ketosis prone diabetes (KPD). These types are characteristically different from one another and include metabolic, pancreatic, and systemic manifestations. Unlike classical type 1 and type 2 diabetes, the subtypes of tropical diabetes possess their own clinical morphologies which are the result of malnutrition, environmental/genetic modification, and pancreatic exocrine dysfunction.^8,10,11

Clinical presentations

General clinical features

This pan disease has four distinct clinical manifestations that differ in subtypes of diabetes. The manifestation of MRDM and FCPD primary deficiency of the pancreatic gland (exocrine) is characterized by loss of fat digestion (steatorrhea), impaired absorption of nutrients (malabsorption), and chronic diarrhoea. In contrast, KPD shows recurrent episodes of diabetic ketoacidosis (DKA) upon insulin dependence.^8,10

Distinctive clinical features of subtypes

Malnutrition-related diabetes mellitus (MRDM)

1. Low Body Mass Index (BMI): Affected individuals often present with BMI <18.5 kg/m², distinguishing it from obesity-driven type 2 diabetes.⁹
2. Insulinopenia without Ketoacidosis: Despite severe insulin deficiency, patients rarely develop DKA, possibly due to residual β-cell function.¹⁰
3. Exocrine Pancreatic Dysfunction: Associated with diarrhea, steatorrhea, and fat-soluble vitamin deficiencies.¹¹
4. Recurrent Abdominal Pain: Patients often report chronic epigastric pain, suggestive of underlying pancreatic pathology.⁸

Fibrocalculous pancreatic diabetes (FCPD)

1. Pancreatic calcifications: Hallmark of FCPD, detected on plain abdominal X-rays or ultrasonography.⁸
2. Postprandial hyperglycemia: Patients often exhibit erratic glucose control with exaggerated postprandial spikes.⁹
3. Exocrine pancreatic insufficiency: Leads to protein and fat malabsorption, often requiring enzyme replacement therapy.¹⁰
4. Absence of autoimmune markers: Unlike type 1 diabetes, FCPD lacks GAD, IA-2, and ZnT8 antibodies.¹¹

Ketosis-prone diabetes (KPD)

1. Episodic DKA: Unlike type 1 diabetes, KPD may not require lifelong insulin therapy.¹⁰
2. Absence of autoimmune markers: Similar to FCPD, KPD lacks autoantibodies associated with type 1 diabetes.⁹
3. Obesity or normal BMI: Unlike MRDM, KPD patients may present with normal or elevated BMI.¹¹
4. Variable β-cell function: Some patients regain near-normal pancreatic function post-DKA episode (Table 3).⁸

Complications of tropical diabetes

Metabolic complications

1. Chronic Hyperglycemia: Leads to microvascular and macrovascular complications similar to classical diabetes.¹⁰
2. Hypoglycemia: Seen in malnourished patients due to poor glycogen stores and limited counter-regulatory hormone response.⁸
3. Electrolyte Imbalances: Chronic diarrhea and poor nutrition contribute to hypokalemia, hyponatremia, and hypomagnesemia.¹¹

 Microvascular complications

1. Diabetic Retinopathy: Prevalence in tropical diabetes patients varies, with FCPD exhibiting higher rates due to chronic hyperglycemia.⁹
2. Diabetic Nephropathy: Renal involvement is more severe in MRDM and FCPD, with early-onset proteinuria and reduced GFR.¹⁰
3. Diabetic Neuropathy: Peripheral and autonomic neuropathy are common, exacerbated by micronutrient deficiencies (e.g., vitamin B12).¹¹

Macrovascular complications

1. Coronary Artery Disease (CAD): A rising concern in tropical diabetes, exacerbated by increasing urbanization and dietary transitions.⁹
2. Peripheral Artery Disease (PAD): More prevalent in malnourished individuals, contributing to non-healing foot ulcers.⁸
   • Pancreatic Complications (Specific to FCPD)
3. Chronic Pancreatitis: Persistent inflammation leads to progressive exocrine and endocrine pancreatic insufficiency.⁹
4. Pancreatic Cancer Risk: FCPD patients may have an elevated risk of pancreatic malignancies.¹⁰ (Table 4) (Graph 1–3).

Graph 1 Distribution of complications across tropical diabetes subtypes.

Graph 2 BMI distribution across diabetes subtypes.

Graph 3 Insulin requirement in tropical diabetes.

Diagnosis and biomarkers of tropical diabetes

The diagnosis of tropical diabetes (TD) is challenging due to multi-faceted factors which includes intermingling symptoms with both type 1 and type 2 diabetes as well as different forms like malnutrition related diabetes mellitus (MRDM), fibrocalculous pancreatic diabetes (FCPD), and even ketosis prone diabetes. Due to the differences in insulin needs and metabolic profile among the subtypes, early and precise determination is critical for proper control.

Clinical and biochemical criteria

Malnutrition-related diabetes mellitus (MRDM)

1. MRDM usually is defined by developed history of malnutrition during early years and has its onset in young adults with low BMI and hyperglycemia.
2. Unlike classical type 1 diabetes, there is an absence of ketosis at diagnosis and like type 2 diabetes, there is mild to moderate obesity and insulin resistance.

Key biochemical markers:

1. Fasting blood glucose (FBG) >126 mg/dL; postprandial blood sugar (PPBG) >200 mg/dL.
2. C-Peptide levels are low to absent which indicate that there is dysfunction of beta cells but no autoimmune destruction.¹
3. Hyperglycaemia with normal to high insulin sensitivity.²

Fibrocalculous pancreatic diabetes (FCPD)

1. For the most part seen in patients who also have chronic pancreatitis and also a history of pancreatic stones.
2. Seen especially in lean persons, it is characterized by increasing beta cell failure in the absence of autoimmune markers.

Key biochemical markers:

1. Exocrine pancreatic insufficiency is indicated by elevated fecal elastase-1.³
2. Increase in serum levels of amylase and lipase during acute exacerbations.
3. Hyperglycemia during fasting is associated with lower levels of C-peptide.⁴

Ketosis-prone diabetes (KPD)  

1. KPD is different from Type 1 diabetes in that many individuals can regain β-cell function post ketoacidosis episodes.
2. Diagnosis is based on the presence of ketosis at onset with varying degree of β cell reserve with time.

Key biomarkers

1. Other than low initial C-peptide, their levels of C-peptide vary post some time which indicates recovery.⁵
2. Auto antibodies such as GAD, IA2 or ZnT8 type are negative making it differ from autoimmune type 1 diabetes.
3. At presentation, more than 9% of glycated haemoglobin (HbA1c) shows strong hyperglycaemia and so does the insulin resistance which is super abundant.⁶

Emerging biomarkers for differentiation  

With the emphasis provided towards accurate classification, new markers have are been proposed:  

Ratios of adiponectin to leptin:

1. FCPD and MRDM patients express lower levels of leptin than Type 2 diabetes which indicates lower adipose tissue mass and is responsible for their diabetes.⁷

Inflammatory and oxidative stress markers:  

1. FCPD patients show high levels of IL-6, TNF-α and other oxidative stress markers due to chronic pancreatitis.
2. KPD have higher levels of CRP which could be associated with inflammation resulting in episodic β-cell dysfunction.

Tests for functional reserve of β-cell:

1. C-peptide test during arginine stimulation is helpful in differentiating KPD patients who can regain β-cell function from those needing insulin therapy for a longer duration.

Epidemiology and public health impact of tropical diabetes

Epidemiology and geographical distribution

With regards to low and middle-income tropical and sub-tropical regions, TD is primarily reported which includes malnutrition related diabetes mellitus (MRDM), fibrocalculous pancreatic diabetes (FCPD) and ketosis prone diabetes (KPD). Due to socioeconomic, nutritional as well as genetic variables, these subtypes prevalence and distribution tend to differ.¹

Malnutrition-related diabetes mellitus (MRDM)

1. Previously documented in South Asia, Sub-Saharan Africa, and Latin America, the MRDM referred to as the 'malnutrition related diabetes mellitus' is a form of diabetes which existed in undernourished populations.²
2. Increased incidence of economic advancement as well as better healthful food options has led to a great decrease of MRDM diabetes, especially within the urban population.³
3. Declining levels of chronic under-nutrition can be observed within MRDM rural, poor communities even today.⁴

Fibrocalculous pancreatic diabetes (FCPD)

1. FCPD has existed in India, Bangladesh, Sri Lanka, and parts of Africa for a long time and is estimated to have a prevalence of 0.5 to 3% in the endemic countries.⁵
2. There is a high association of chronic cassava eating (which is high in cyanogenic glycosides) and FCPD, especially in certain rural areas.⁶
3. Some researchers argue that genetic factors, like mutations in SPINK1, can help explain the regional concentration of FCPD cases.⁷

Ketosis-prone diabetes (KPD)

1. The condition is most frequently noted in African, Hispanic, and South Asian groups and is one of the most common causes of diabetes mellitus related ketoacidosis in these regions.²
2. Unlike with type 1 diabetes, many patients with KPD recompose their b-cell mass and functionality, suggesting that there is an environmentally and genetically influenced region specific metabolic disease.³
3. Transformations in nutrition and migration from rural to urban areas have been linked with increased prevalence of KPD, especially among young adults.⁶

Public health impact

Economic burden

1. Managing TD is costlier than it should be because of its relatin to poverty, undernutrition, and poor health care access.⁵
2. Many patients dependent on insulin therapy need to continue with it for life, which is not feasible economically in lower middle income settings.⁴

Healthcare Challenges

1. Delayed or inappropriate treatment of tropical diabetes is common due to its frequent misdiagnosis and misclassification.¹
2. Limited access to health care infrastructure makes it difficult to obtain diagnostic tests like pancreatic imaging and C-peptide assays for accurate classification.²

Nutrition and lifestyle shifts

1. The rise of KPD and FCPD diabetes reflects a nutrition transition and is in contrast to the lowered prevalence of MRDM in urban areas.³
2. Changes in the epidemiology of diabetes in tropical countries is being fueled by increased consumption of processed food, reduced physical activity, and increasing obesity.⁶

Need for public health interventions

1. Detection of the disease can be improved with early screening programs for systematically malnourished or suffering from recurrent pancreatitis coupled with unexplained ketoacidosis.
2. Initiatives to provide affordable insulin are needed to properly manage cases with FCPD and insulin dependent MRDM.⁷
3. Policies aimed at reducing undernutrition coupled with dietary toxins like those containing cyanogenic compounds should be strengthened to aid in preventing FCPD.

Challenges and future directions

The challenges tropical diabetes poses with its accurate diagnosis, classification, and management, is especially heightened in the case of limited resources where biochemical and imaging tools remain advanced and out of reach.^1–3 In addition, the overlap of MRDM, FCPD, and KPD with type one and two diabetes further complicates clinical decision making, causing misdiagnosis and poor treatment approaches. Type 1 and type 2 diabetes and its multiple forms lead to overwhelming clinical ambiguity which leads to inadequate detection and subpar treatment plans.^4–6 Moreover, the socioeconomic irresponsibility gives rise to an increased cost burden for managing insulin dependent cases especially in FCPD and severe MRDM.^7,8 Research should be directed towards standardizing the criteria for diagnosis, biomarker-based classification, and their focus should also be on precision medicine to cater to the metabolic diversity tropical diabetes has on offer.^9,10 Moreover, there is a need for public health action aimed at the deeply rooted cyanogen and chronic malnutrition exposures which aid in the contribution to FCPD and MRDM.¹¹

“In resource-constrained settings, management of FCPD and insulin-dependent MRDM often involves a pragmatic combination of low-dose basal insulin and oral agents such as metformin or sulfonylureas. This approach has been shown to improve glycemic control while mitigating the cost and compliance barriers associated with full insulin therapy. However, randomized studies validating this strategy are still lacking.”^12–15

Given the development of malnutrition-related diabetes mellitus, fibrocalculous pancreatic diabetes, and ketosis-prone diabetes, tropical diabetes is associated with an emerging range of diabetes subtypes. These forms, unlike classical type 1 and 2 diabetes, are characterized by nutritionally deficient and pancreatic exocrine deficient features superimposed on aetiological, clinical and metabolic features.^1–3 Although the prevalence of MRDM was reduced with the economic advancement and better nutrition, FCPD, and KPD remain prominent problems especially in the tropics and sub tropics where dietary harmful substances along with chronic pancreatitis and metabolic changes are some of the causative factors.^4–6 Prolonged discrimination and inaccessibility to advanced biomarkers, pancreatic imaging, and C-peptide diagnostic modalities have resulted to inaccurate diagnosis and subsequently mismanaged treatment, thus remains the most significant challenge.^7–9 In addition, the absence of equity in health care delivery, expensive treatment processes as well as unorganized managing systems all amplify the problems attending tropical diabetes.^10,11 These issues need to be tackled from multiple perspectives such as implementing screening programs at an earlier age, providing inexpensive insulin, integration of precision medicine, and educating the public to eliminate the cases of malnutrition and health damaging food intake.

“There is an urgent need for randomized controlled trials to optimize treatment algorithms for tropical diabetes phenotypes, particularly in populations with overlapping malnutrition and exocrine pancreatic dysfunction. Parallelly, public health policy reforms must address the socioeconomic and nutritional determinants that fuel this unique diabetes spectrum.”

Focused genetic and metabolic markers with better classification systems combined with targeted treatment options is what the future should fuse to best optimize management strategies in the seemingly diverse populations.

A case in point is that, with good epidemiology, clinical, and public health integration, disease management for tropical diabetes can be enhanced and patient outcomes improved in the respective areas.

“The upcoming International Diabetes Federation (IDF) Working Group guidelines on Type 5 Diabetes, expected in 2027, may serve as a much-needed consensus document for defining diagnostic criteria and therapeutic strategies tailored to tropical diabetes.”

None.

The author declares that there are no conflicts of interest.

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