Diabetes Mellitus and Hypercalcaemia Case Study

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4th Oct 2017 Health Reference this

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ABSTRACT

We report a case of diabetes mellitus in a middle aged female who developed primary hyperparathyroidism and had parathyroidectomy. She had multiple hospitalizations for vomiting, pain abdomen and dehydration. Hypercalcaemia was never documented though. She developed pancreatic calcification later, was diagnosed as FCPD (Fibrocalculupancreatic diabetes) and treated with insulin. In the next hospitalization, nephrolithiasis, hypercalcaemia and high PTH (parathormone) levels were detected. A solitary parathyroid adenoma was identified and surgically removed. Gastrointestinal symptoms disappeared but diabetes remained unaltered

keywords: Diabetes, Hypercalcaemia, Parathyroid adenoma

INTRODUCTION

Pancreatic calcification is a well recognized cause of diabetes but development of primary hyperparathyroidism in the background of pancreatic and renal calcification and diabetes is uncommon. Solitary parathyroid adenomas are the commonest cause of primary hyperparathyroidism. Primary hyperparathyroidism classically presents with fractures, kidney stones, depression, hypertension and peptic ulcer disease, predominantly in females. Clinical presentation of primary hyperparathyroidism is changing and most cases are now picked up during evaluation of other conditions. We report a case of primary hyperparathyroidism who presented with gastrointestinal symptoms followed by multiorgan calcification and then diabetes and finally life threatening hypercalcaemia..

CASE REPORT

Mrs. T C, 51 –year-old female had recurrent episodes of vomiting with dehydration necessitating multiple (2 to 3 times every year) episodes of hospitalization since 1988. No surgical cause could be identified. Initial investigations in 1988 revealed plasma glucose, calcium, phosphorus, liver function tests, serum amylase, lipase all within normal limits. Ultrasonography of pancreas, upper GI endoscopy and CT scan of abdomen were normal.

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The patient developed diabetes in 1991, during the course of a hospital admission. Her serum amylase level was 47 iu/l (within normal range); sonography of the abdomen showed pancreatic calcification and a CT scan showed pancreatic calcification with dilated pancreatic duct, intraductal calculi and atrophic pancreas suggestive of chronic pancreatitis. From 1993 the intensity and frequency of episodic vomiting and pain abdomen increased, occurring every 3-4 months and relieved gradually over 3-4 days with iv fluids and conservative management.

In 2003 she was hospitalized with urinary tract infection and was found to have hypertension and bilateral nephrolithiasis. At that time, her diabetes was poorly controlled (FPG : 230 mg/dl, PPPG : 245 mg / dl), normal renal profile (urea : 25 mg/dl, creatinine : 0.86 mg/dl) and normal serum calcium (9.12 mg /dl). She was discharged after stabilization with insulin.

In December 2004, she was admitted to hospital with similar symptoms along with severe hyperglycaemia (365mg/dl). Investigations revealed, no ketone bodies in urine, normal amylase (29 iu/l) and lipase (14 iu/l ). There were multiple areas of calcification in pancreas, spleen, kidneys on sonography. Her renal profile was normal (Urea : 44 mg / dl, Creatinine : 1.2 mg/dl) with severe hypercalcaemia (serum calcium : more than 15 mg/dl) and normal serum phosphorus (4.7 mg/dl) and albumin (4.0 gm/dl ).

Initially hypercalcaemia was treated with iv saline and oral alendronate. Her calcium came down to 9.4mg/dl and phosphorus came to 0.6mg/dl and then the latter stabilized at 10mg/dl and 3.44mg/dl respectively. Her serum PTH level was high at 221.7 pg/ml (normal range : 11–79.5pg/ml), obtained at a time when serum calcium had normalized at 10.0 mg/dl. She was advised a parathyroid sestamibi scan which showed a right inferior parathyroid adenoma.

The patient underwent right inferior parathyroidectomy. Histology confirmed a parathyroid adenoma. Following parathyroid surgery her gastrointestinal symptoms disappeared but diabetes persisted and required insulin. Her serum calcium and phosphate levels were normal (Ca : 8.58 mg/dl & PO4 : 3.54 mg/dl) with oral calcium : 1.5gm daily and Calcitriol : 0.5ug daily.

She was further evaluated for MEN1, but no pituitary pathology was seen on CT scan. She is on regular follow up till March 2012 and requires insulin treatment regularly for control of the persistent hyperglycemic state.

DISCUSSION

Primary hyperparathyroidism (PHPT) has a variable clinical expression. The clinical profile of the disease in West has changed from that described in the past but symptomatic PHPT is still the predominant form of the disease in many parts of the world, especially developing countries .1 PHPT in Indians is a severe, symptomatic disorder with skeletal, muscular and renal manifestations at a younger age.2

Our patient presented with gastrointestinal symptoms first (1988), pancreatic calcification & diabetes (1991 ) second, nephrolithiasis (2003) third and life threatening hypercalcaemia (2004) at the last. Intermittent hypercalcaemia is a recognized biochemical finding of PHPT3 and often require very sophisticated diagnostic tools (parathyroid venous sampling and bone densitometry) to identify the cause4 at this early stage of the disease. Intermittent hypercalcaemia may be the cause of repeated attacks of vomiting and pain abdomen in the initial years.

Intermittent hypercalcaemia may produce multiorgan calcification including kidney5 before development of symptomatic hypercalcaemia. Parathyroid adenoma may lead to pancreatic calcification6 and PHPT leading to pancreatic calcification can give rise to diabetes.7

Increased prevalence of diabetes mellitus (DM) and glucose intolerance in primary hyperparathyroidism (PHPT) is established by many studies.8,9 The prevalence of diabetes mellitus in primary hyperparathyroidism is approximately 8% and that of primary hyperparathyroidism in diabetic patients is approximately 1%. Both values are about three-fold higher than the respective expected prevalences in general populations.10 In our given case diabetes and pancreatic calcification developed early (in 1991 ) and hypercalcemia with PHPT discovered 13 years later (in 2004).

The response of parathyroid surgery on diabetes is variable : diabetic condition improves or cured in some patients,10 remain unaltered in another some and some patients experienced a deterioration of their glucose tolerance.11 Diabetic state of our given patient remained unaltered following parathyroid surgery. The type of diabetes associated with PHPT is also variable. Type1 or Type 210,13 or may be a secondary diabetes from pancreatic calcification.7 A diagnosis of chronic calcific pancreatitis (CCP) was established in this patient by evidence of characteristic abdominal pain; presence of diabetes mellitus and radiological evidence of pancreatic calculi.12

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MEN : MEN1 is characterized by the combined occurrence of tumors of the parathyroid, pancreatic islet cells and anterior pituitary. Parathyroid tumors occur in 95% of MEN1 patients and the resulting hypercalcaemia is the first manifestation in about 90% of patients. Though no neoplastic changes was identified in pituitary or pancreatic region of the patient, a close follow up necessary to detect such changes in future.

MEN2 describes the association of medullary thyroid carcinoma , pheochromocytomas and parathyroid tumors. Medullary thyroid carcinoma is the commonest component in MEN2. The patient had no goitre and serum calcitonin level could not be estimated.

CONCLUSION

Hyperparathyroidism may not be associated with persistent hypercalcaemia, but rather present as intermittent or episodic high serum calcium levels. Our case study underlines the importance of considering hypercalcaemia if a patient presents with recurrent GI (gastrointestinal) symptoms. Hypercalcaemia may also lead to multiple organ calcifications. The high Ca (calcium) levels and GI symptoms may resolve with parathyroidectomy, but the irreversible diabetes persists.

REFERENCES

1. Bhansali A, Masoodi SR, Reddy KS, et al. Primary hyperparathyroidism in North India: A description of 52 cases. Ann Saudi Med. 2005; 25(1):29-35.

2. Mishra SK, Agarwal G, Kar DK, et al. Unique clinical characteristics of Primary hyperparathyroidism in India. Br J Surg. 2001; 88(5):708-14.

3. Broadus AE, Horst RL, Littledike ET, et al. Primary hyperparathyroidism with intermittent hypercalcaemia: serial observations and simple diagnosis by means of an oral calcium tolerance tests. Clin Endocrinol (Oxf). 1980; 12(3):225-35.

4. Barilla DE, Pak CY. Pitfalls in parathyroid evaluation in patients with calcium urolithiasis. Urol Res. 1979; 7(3):177-82.

5. Ljunghall S, Kallsen R, Backman U, et al. Clinical effects of parathyroid surgery in normocalcaemic patients with recurrent renal stones. Acta Chir Scand. 1980; 146(3):161-9.

6. Stone GR. Pancreas and parathyroid. Parathyroid adenoma in association with pancreatic calcification. J Kans Med Soc. 1962 Dec; 63:519-21.

7. Kubota S, Yamada Y, Wakasugi H, et al. An autopsy case of renal failure as its cause of death in a patient with primary hyperparathyroidism associated with chronic pancreatitis. Fukuoka Igaku Zasshi. 1996; 87(10):226-8.

8. Taylor WH. The prevalence of diabetes mellitus in patients with hyperparathyroidism and among their relatives. Diabet Med 1991; 8: 683-687.

9. Khaleeli AA, Johnson JN, Taylor WH. Prevalence of glucose intolerance in primary hyperparathyroidism and the benefit of parathyroidectomy. Diabetes Metab Res Rev. 2007; 23(1):43-8.

10. Taylor WH, Khaleeli AA. Coincident diabetes mellitus and primary hyperparathyroidism. Diabetes Metab Res Rev. 2001; 17(3):175-80.

11. Ljunghall S, Palmer M, Akerstrom, G et al. Diabetes mellitus, glucose tolerance and insulin response to glucose in patients with primary hyperparathyroidism before and after parathyroidectomy. Eur J Clin Invest. 1983; 13(5):373-7.

12. Balaji LN, Tandon RK, Tandon BN, et al. Prevalence and clinical features of chronic pancreatitis in southern India. Int J Pancreatol. 1994; 15(1):29-34.

ABSTRACT

We report a case of diabetes mellitus in a middle aged female who developed primary hyperparathyroidism and had parathyroidectomy. She had multiple hospitalizations for vomiting, pain abdomen and dehydration. Hypercalcaemia was never documented though. She developed pancreatic calcification later, was diagnosed as FCPD (Fibrocalculupancreatic diabetes) and treated with insulin. In the next hospitalization, nephrolithiasis, hypercalcaemia and high PTH (parathormone) levels were detected. A solitary parathyroid adenoma was identified and surgically removed. Gastrointestinal symptoms disappeared but diabetes remained unaltered

keywords: Diabetes, Hypercalcaemia, Parathyroid adenoma

INTRODUCTION

Pancreatic calcification is a well recognized cause of diabetes but development of primary hyperparathyroidism in the background of pancreatic and renal calcification and diabetes is uncommon. Solitary parathyroid adenomas are the commonest cause of primary hyperparathyroidism. Primary hyperparathyroidism classically presents with fractures, kidney stones, depression, hypertension and peptic ulcer disease, predominantly in females. Clinical presentation of primary hyperparathyroidism is changing and most cases are now picked up during evaluation of other conditions. We report a case of primary hyperparathyroidism who presented with gastrointestinal symptoms followed by multiorgan calcification and then diabetes and finally life threatening hypercalcaemia..

CASE REPORT

Mrs. T C, 51 –year-old female had recurrent episodes of vomiting with dehydration necessitating multiple (2 to 3 times every year) episodes of hospitalization since 1988. No surgical cause could be identified. Initial investigations in 1988 revealed plasma glucose, calcium, phosphorus, liver function tests, serum amylase, lipase all within normal limits. Ultrasonography of pancreas, upper GI endoscopy and CT scan of abdomen were normal.

The patient developed diabetes in 1991, during the course of a hospital admission. Her serum amylase level was 47 iu/l (within normal range); sonography of the abdomen showed pancreatic calcification and a CT scan showed pancreatic calcification with dilated pancreatic duct, intraductal calculi and atrophic pancreas suggestive of chronic pancreatitis. From 1993 the intensity and frequency of episodic vomiting and pain abdomen increased, occurring every 3-4 months and relieved gradually over 3-4 days with iv fluids and conservative management.

In 2003 she was hospitalized with urinary tract infection and was found to have hypertension and bilateral nephrolithiasis. At that time, her diabetes was poorly controlled (FPG : 230 mg/dl, PPPG : 245 mg / dl), normal renal profile (urea : 25 mg/dl, creatinine : 0.86 mg/dl) and normal serum calcium (9.12 mg /dl). She was discharged after stabilization with insulin.

In December 2004, she was admitted to hospital with similar symptoms along with severe hyperglycaemia (365mg/dl). Investigations revealed, no ketone bodies in urine, normal amylase (29 iu/l) and lipase (14 iu/l ). There were multiple areas of calcification in pancreas, spleen, kidneys on sonography. Her renal profile was normal (Urea : 44 mg / dl, Creatinine : 1.2 mg/dl) with severe hypercalcaemia (serum calcium : more than 15 mg/dl) and normal serum phosphorus (4.7 mg/dl) and albumin (4.0 gm/dl ).

Initially hypercalcaemia was treated with iv saline and oral alendronate. Her calcium came down to 9.4mg/dl and phosphorus came to 0.6mg/dl and then the latter stabilized at 10mg/dl and 3.44mg/dl respectively. Her serum PTH level was high at 221.7 pg/ml (normal range : 11–79.5pg/ml), obtained at a time when serum calcium had normalized at 10.0 mg/dl. She was advised a parathyroid sestamibi scan which showed a right inferior parathyroid adenoma.

The patient underwent right inferior parathyroidectomy. Histology confirmed a parathyroid adenoma. Following parathyroid surgery her gastrointestinal symptoms disappeared but diabetes persisted and required insulin. Her serum calcium and phosphate levels were normal (Ca : 8.58 mg/dl & PO4 : 3.54 mg/dl) with oral calcium : 1.5gm daily and Calcitriol : 0.5ug daily.

She was further evaluated for MEN1, but no pituitary pathology was seen on CT scan. She is on regular follow up till March 2012 and requires insulin treatment regularly for control of the persistent hyperglycemic state.

DISCUSSION

Primary hyperparathyroidism (PHPT) has a variable clinical expression. The clinical profile of the disease in West has changed from that described in the past but symptomatic PHPT is still the predominant form of the disease in many parts of the world, especially developing countries .1 PHPT in Indians is a severe, symptomatic disorder with skeletal, muscular and renal manifestations at a younger age.2

Our patient presented with gastrointestinal symptoms first (1988), pancreatic calcification & diabetes (1991 ) second, nephrolithiasis (2003) third and life threatening hypercalcaemia (2004) at the last. Intermittent hypercalcaemia is a recognized biochemical finding of PHPT3 and often require very sophisticated diagnostic tools (parathyroid venous sampling and bone densitometry) to identify the cause4 at this early stage of the disease. Intermittent hypercalcaemia may be the cause of repeated attacks of vomiting and pain abdomen in the initial years.

Intermittent hypercalcaemia may produce multiorgan calcification including kidney5 before development of symptomatic hypercalcaemia. Parathyroid adenoma may lead to pancreatic calcification6 and PHPT leading to pancreatic calcification can give rise to diabetes.7

Increased prevalence of diabetes mellitus (DM) and glucose intolerance in primary hyperparathyroidism (PHPT) is established by many studies.8,9 The prevalence of diabetes mellitus in primary hyperparathyroidism is approximately 8% and that of primary hyperparathyroidism in diabetic patients is approximately 1%. Both values are about three-fold higher than the respective expected prevalences in general populations.10 In our given case diabetes and pancreatic calcification developed early (in 1991 ) and hypercalcemia with PHPT discovered 13 years later (in 2004).

The response of parathyroid surgery on diabetes is variable : diabetic condition improves or cured in some patients,10 remain unaltered in another some and some patients experienced a deterioration of their glucose tolerance.11 Diabetic state of our given patient remained unaltered following parathyroid surgery. The type of diabetes associated with PHPT is also variable. Type1 or Type 210,13 or may be a secondary diabetes from pancreatic calcification.7 A diagnosis of chronic calcific pancreatitis (CCP) was established in this patient by evidence of characteristic abdominal pain; presence of diabetes mellitus and radiological evidence of pancreatic calculi.12

MEN : MEN1 is characterized by the combined occurrence of tumors of the parathyroid, pancreatic islet cells and anterior pituitary. Parathyroid tumors occur in 95% of MEN1 patients and the resulting hypercalcaemia is the first manifestation in about 90% of patients. Though no neoplastic changes was identified in pituitary or pancreatic region of the patient, a close follow up necessary to detect such changes in future.

MEN2 describes the association of medullary thyroid carcinoma , pheochromocytomas and parathyroid tumors. Medullary thyroid carcinoma is the commonest component in MEN2. The patient had no goitre and serum calcitonin level could not be estimated.

CONCLUSION

Hyperparathyroidism may not be associated with persistent hypercalcaemia, but rather present as intermittent or episodic high serum calcium levels. Our case study underlines the importance of considering hypercalcaemia if a patient presents with recurrent GI (gastrointestinal) symptoms. Hypercalcaemia may also lead to multiple organ calcifications. The high Ca (calcium) levels and GI symptoms may resolve with parathyroidectomy, but the irreversible diabetes persists.

REFERENCES

1. Bhansali A, Masoodi SR, Reddy KS, et al. Primary hyperparathyroidism in North India: A description of 52 cases. Ann Saudi Med. 2005; 25(1):29-35.

2. Mishra SK, Agarwal G, Kar DK, et al. Unique clinical characteristics of Primary hyperparathyroidism in India. Br J Surg. 2001; 88(5):708-14.

3. Broadus AE, Horst RL, Littledike ET, et al. Primary hyperparathyroidism with intermittent hypercalcaemia: serial observations and simple diagnosis by means of an oral calcium tolerance tests. Clin Endocrinol (Oxf). 1980; 12(3):225-35.

4. Barilla DE, Pak CY. Pitfalls in parathyroid evaluation in patients with calcium urolithiasis. Urol Res. 1979; 7(3):177-82.

5. Ljunghall S, Kallsen R, Backman U, et al. Clinical effects of parathyroid surgery in normocalcaemic patients with recurrent renal stones. Acta Chir Scand. 1980; 146(3):161-9.

6. Stone GR. Pancreas and parathyroid. Parathyroid adenoma in association with pancreatic calcification. J Kans Med Soc. 1962 Dec; 63:519-21.

7. Kubota S, Yamada Y, Wakasugi H, et al. An autopsy case of renal failure as its cause of death in a patient with primary hyperparathyroidism associated with chronic pancreatitis. Fukuoka Igaku Zasshi. 1996; 87(10):226-8.

8. Taylor WH. The prevalence of diabetes mellitus in patients with hyperparathyroidism and among their relatives. Diabet Med 1991; 8: 683-687.

9. Khaleeli AA, Johnson JN, Taylor WH. Prevalence of glucose intolerance in primary hyperparathyroidism and the benefit of parathyroidectomy. Diabetes Metab Res Rev. 2007; 23(1):43-8.

10. Taylor WH, Khaleeli AA. Coincident diabetes mellitus and primary hyperparathyroidism. Diabetes Metab Res Rev. 2001; 17(3):175-80.

11. Ljunghall S, Palmer M, Akerstrom, G et al. Diabetes mellitus, glucose tolerance and insulin response to glucose in patients with primary hyperparathyroidism before and after parathyroidectomy. Eur J Clin Invest. 1983; 13(5):373-7.

12. Balaji LN, Tandon RK, Tandon BN, et al. Prevalence and clinical features of chronic pancreatitis in southern India. Int J Pancreatol. 1994; 15(1):29-34.

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