2016
LETTERS TO THE EDITOR
late.4,7 As in the case described herein, hypoglycemia and hyponatremia are common sequelae.8 Although the prevalence of hypopituitarism in old age is unknown, physicians should consider its possibility when examining for failure to thrive and frailty syndromes. The most commonly assumed explanation for wrinkled skin, lethargy, and incontinence infrequently leads to diagnosis, and pituitary tumors are surprisingly common findings at autopsy.9 Tumor resection, thyroid replacement, and corticosteroid therapy generally yield good results in elderly adults. Medical therapy is often sufficient in improving symptoms and function. Because cardiovascular mortality is higher in individuals with untreated hypopituitarism than in the rest of the population, treatment may lengthen life.10 Individuals with physical limitations such as flexion contractures have shown complete reversal. The restoration of quality of life is a meaningful goal making examination for hypopituitarism equally worthwhile. Stacey Ruff, DO Khaled Imam, MD Department of Geriatrics, William Beaumont Hospital Royal Oak, Michigan Beaumont Geriatric Assessment Center, Berkley, Michigan William Beaumont School of Medicine, Oakland University, Rochester, Michigan Woodward Hills Nursing Center, Bloomfield Hills Michigan
ACKNOWLEDGMENTS Conflict of Interest: The editor in chief has reviewed the conflict of interest checklist provided by the authors and has determined that the authors have no financial or any other kind of personal conflicts with this paper. Author Contributions: Both authors contributed to this paper. Sponsor’s Role: None.
REFERENCES 1. Belchetz PE. Idiopathic hypopituitarism in the elderly. Br Med J 1985;291:247–248. 2. Regal M, Paramo C, Sierra SM et al. Prevalence and incidence of hypopituitarism in adult Caucasian population in northwestern Spain. Clin Endocrinol 2001;55:735–740. 3. Schneider HJ, Kreitschmann-Andermahr I, Ghigo E et al. Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: A systematic review. JAMA 2007;298:1429–1438. 4. Tayal SC, Bansal SK, Chadha DK. Hypopituitarism: A difficult diagnosis in elderly people but worth a search. Age Ageing 1994;23:320–322. 5. Sarkisian CA, Lachs MS. Failure to thrive in older adults. Ann Intern Med 1996;124:1072–1078. 6. Verdary RB. Failure to thrive in the elderly. Clin Ger Med 1995;11:653–659. 7. Foppiani L, Ruelle A, Bandelloni R et al. Hypopituitarism in the elderly: Multifaceted clinical and biochemical presentation. Curr Aging Sci 2008;1:42–50. 8. Asano T, Aoki A, Sasaki M et al. Hyponatremia is the valuable manifestation for initiating diagnosis of hypopituitarism in the elderly. Endocr J 2012;59:1015–1020. 9. Kovacs K, Ryan N, Horvath E et al. Pituitary adenomas in old age. J Gerontol 1980;35:16–22. 10. Foppiani L, Ruelle A, Quilici P et al. Hypopituitarism in the elderly: Two case-reports with heterogeneous presentation. Aging Clin Exp Res 2009;21:76–81.
OCTOBER 2014–VOL. 62, NO. 10
JAGS
EOSINOPHILIC COLITIS: A RARE CAUSE OF LOWER GASTROINTESTINAL BLEEDING IN AN ELDERLY ADULT To the Editor: Lower gastrointestinal bleeding (LGIB) affects a significant number of elderly adults and is an important cause of morbidity and mortality. The incidence of LGIB increases with age and is more common in men than women.1 Reviewing the literature, LGIB associated with eosinophilic colitis in an elderly adult has never been reported. Herein is presented a 77-year-old woman with LGIB due to eosinophilic colitis (EC) who was successfully treated with prednisone and azathioprine. The woman was admitted to the hospital with complaints of rectal bleeding and abdominal pain. She had a 20-year history of hypertension. Laboratory findings were serum hemoglobin 6.7 g/dL, white cell count 12,500/lL with 20% eosinophils (eosinophil count 2,500/lL) and platelet count 240,000/lL. Biochemical tests were within normal limits. History revealed no allergic disease, food or drug allergy, or use of antibiotics. Physical examination was unremarkable except for diffuse abdominal tenderness. Colonoscopy showed two rectal ulcers 22 and 12 mm in diameter. Multiple biopsies were taken (Figure 1). Histopathological examination of rectal ulcers showed active inflammatory reaction with focal clusters of eosinophils in lamina propria consistent with EC. Prednisone 40 mg/d and azathioprine 100 mg/d were started, and her symptoms, including rectal bleeding and abdominal pain, resolved within 2 weeks. Four weeks after discharge from the hospital, colonoscopy was normal and she no longer had any symptoms. EC is a rare clinical condition that most frequently affects neonates and young adults. Clinical presentation of EC is usually nonspecific and depends on the layer of intestinal wall that eosinophils have infiltrated. Abdominal pain, nonbloody and bloody diarrhea, and significant weight loss are the hallmarks of EC.2 EC may also present acutely and lead to severe and fatal complications such as hemorrhage and perforation.3 Two neonates with LGIB due to EC have been reported in the literature. The authors suggested that infiltrated eosinophils in the colonic mucosa could be involved in the pathogenesis of LGIB.4
Figure 1. Colonoscopic examination revealed the white base of a 12-mm-long rectal ulcer (black arrow).
JAGS
OCTOBER 2014–VOL. 62, NO. 10
Eosinophilic colitis is a rare clinical condition, so the most important factor in making the diagnosis is to have a high degree of clinical suspicion. In conclusion, clinicians should consider EC in the differential diagnosis of LGIB in elderly adults, and early medical treatment should be initiated to avoid serious complications. G€ ulay Kocßak, MD Department of Nephrology, C ß anakkale Onsekiz Mart University, C ß anakkale, Turkey Erdem Kocßak, MD Department of Gastroenterology, C ß anakkale State Hospital, C ß anakkale, Turkey Erdem Akbal, MD Department of Gastroenterology, C ß anakkale Onsekiz Mart University, C ß anakkale, Turkey Hacer Sßen, MD G€ okhan Erba g, MD Ceren Erdo gan, MD Department of Internal Medicine, C ß anakkale Onsekiz Mart University, C ß anakkale, Turkey
ACKNOWLEDGMENTS Conflict of Interest: The editor in chief has reviewed the conflict of interest checklist provided by the authors and has determined that the authors have no financial or any other kind of personal conflicts with this paper. Author Contributions: G€ ulay Kocßak: manuscript concept and design. Erdem Kocßak, G€ okhan Erba g: preparation of manuscript. Erdem Akbal, Hacer Sßen: analysis and interpretation of data. Ceren Erdo gan: subject’s doctor. Sponsor’s Role: No sponsor associated with manuscript.
REFERENCES 1. Chait MM. Lower gastrointestinal bleeding in the elderly. World J Gastrointest Endosc 2010;2:147–154. 2. Alfadda AA, Schaffer EA, Urbanski SJ et al. Eosinophilic colitis is a sporadic self-limited disease of middle-aged people: A population-based study. Colorectal Dis 2014;16:123–129. 3. Yeo SA, Lim YK, Lim KH et al. Toxic haemorrhagic colitis: A rare presentation of eosinophilic colitis. Case Rep Gastrointest Med 2012;2012: 279813. 4. Ohtsuka Y, Shimizu T, Shoji H et al. Neonatal transient eosinophilic colitis causes lower gastrointestinal bleeding in early infancy. J Pediatr Gastroenterol Nutr 2007;44:501–505.
CASE REPORT: SENILE-ONSET AMYLOIDOSIS PRESENTING WITH PAINFUL LOWER EXTREMITY NEUROPATHY To the Editor: Peripheral neuropathy symptomatology ranges from intermittent numbness to constant burning with muscle weakness. Neuropathy interferes with postural control and is a risk factor for falls1 in community-dwelling elderly adults. Identifying the etiology of peripheral neuropathy in elderly adults is challenging because they often have multiple comorbid conditions that may
LETTERS TO THE EDITOR
2017
contribute to the development of this disorder. Pinpointing the cause, such as in senile-onset amyloidosis, whose incidence in elderly adults is unknown and whose prevalence increases with age (seen in 25% of 80-year-olds),2 can help prevent further nerve damage, disability, and falls and help clinicians inform people on their likely prognosis. A high-functioning 73-year-old man presented for an initial geriatric consultation complaining of 12-year progressive lower extremity neuropathic pain accompanied by weakness and imbalance. He had undergone multiple evaluations and was comanaged by staff in a pain clinic using pharmacological and nonpharmacological approaches with the working diagnosis of idiopathic peripheral sensory neuropathy with paresthesias for longer than 5 years. He also complained of dyspnea on exertion for a few months without chest pain or palpitations. His medical history included diabetes mellitus, hypothyroidism, coronary artery disease (CAD), previous myocardial infarction, pacemaker placement, anterior cervical fusion, and bilateral carpal tunnel release in 1998 and 2003. The man was married and employed as a college football coach. He was independent in basic and instrumental activities of daily living. He had a family history of early CAD in his father and brother. On physical examination, his lower extremities had 1+ edema, diminished sensation to monofilament, diminished vibratory sense, dystrophic toenails, palpable pulses, no gross deformity, and intact skin. Cranial nerves were intact, with normal tone, bulk, and strength in his extremities. Reflexes were 1+ except 0 at the Achilles tendon. Romberg was positive. His gait was wide-based and ataxic on tandem walking. His heart rate and rhythm were regular without a third heart sound, and his jugular venous distention was measured at 12 cm. Cognitive testing was normal. Laboratory testing revealed serum protein electrophoresis with no M-protein, a urine protein electrophoresis with trace proteinuria, and free light chains with free kappa of 23.7 and free lambda of 22.6 with a normal K/L ratio. Bone marrow biopsy was negative. Nerve conduction study in 2001 revealed mild demyelination and axonopathy. Subsequent studies, in 2008 and 2012, revealed dramatic progression of a severe sensorimotor axonopathy with demyelinating features and absent lower extremity sensory nerve action potentials (SNAPs). An echocardiogram showed thickening of the left ventricular wall and worsening diastolic filling consistent with restriction. Electrocardiograms revealed low-voltage QRS complexes from 2005 to 2012. He underwent cardiac muscle biopsy, which revealed amorphous eosinophilic deposition that Congo red staining confirmed to be amyloid. Because immunostains for classification of subtypes were unrevealing, further subtype investigation was undertaken with transthyretin (TTR) genetic analysis.
DISCUSSION Amyloidosis results from protein misfolding and deposition within tissues. As a result, neuropathy often presents as a progressive, symmetric, axonal disease of the distal lower extremities with prominent small fiber features, ultimately affecting motor and sensory fibers, decreased SNAPs, and relatively normal conduction velocities.3 The cause of
LETTERS TO THE EDITOR
late.4,7 As in the case described herein, hypoglycemia and hyponatremia are common sequelae.8 Although the prevalence of hypopituitarism in old age is unknown, physicians should consider its possibility when examining for failure to thrive and frailty syndromes. The most commonly assumed explanation for wrinkled skin, lethargy, and incontinence infrequently leads to diagnosis, and pituitary tumors are surprisingly common findings at autopsy.9 Tumor resection, thyroid replacement, and corticosteroid therapy generally yield good results in elderly adults. Medical therapy is often sufficient in improving symptoms and function. Because cardiovascular mortality is higher in individuals with untreated hypopituitarism than in the rest of the population, treatment may lengthen life.10 Individuals with physical limitations such as flexion contractures have shown complete reversal. The restoration of quality of life is a meaningful goal making examination for hypopituitarism equally worthwhile. Stacey Ruff, DO Khaled Imam, MD Department of Geriatrics, William Beaumont Hospital Royal Oak, Michigan Beaumont Geriatric Assessment Center, Berkley, Michigan William Beaumont School of Medicine, Oakland University, Rochester, Michigan Woodward Hills Nursing Center, Bloomfield Hills Michigan
ACKNOWLEDGMENTS Conflict of Interest: The editor in chief has reviewed the conflict of interest checklist provided by the authors and has determined that the authors have no financial or any other kind of personal conflicts with this paper. Author Contributions: Both authors contributed to this paper. Sponsor’s Role: None.
REFERENCES 1. Belchetz PE. Idiopathic hypopituitarism in the elderly. Br Med J 1985;291:247–248. 2. Regal M, Paramo C, Sierra SM et al. Prevalence and incidence of hypopituitarism in adult Caucasian population in northwestern Spain. Clin Endocrinol 2001;55:735–740. 3. Schneider HJ, Kreitschmann-Andermahr I, Ghigo E et al. Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: A systematic review. JAMA 2007;298:1429–1438. 4. Tayal SC, Bansal SK, Chadha DK. Hypopituitarism: A difficult diagnosis in elderly people but worth a search. Age Ageing 1994;23:320–322. 5. Sarkisian CA, Lachs MS. Failure to thrive in older adults. Ann Intern Med 1996;124:1072–1078. 6. Verdary RB. Failure to thrive in the elderly. Clin Ger Med 1995;11:653–659. 7. Foppiani L, Ruelle A, Bandelloni R et al. Hypopituitarism in the elderly: Multifaceted clinical and biochemical presentation. Curr Aging Sci 2008;1:42–50. 8. Asano T, Aoki A, Sasaki M et al. Hyponatremia is the valuable manifestation for initiating diagnosis of hypopituitarism in the elderly. Endocr J 2012;59:1015–1020. 9. Kovacs K, Ryan N, Horvath E et al. Pituitary adenomas in old age. J Gerontol 1980;35:16–22. 10. Foppiani L, Ruelle A, Quilici P et al. Hypopituitarism in the elderly: Two case-reports with heterogeneous presentation. Aging Clin Exp Res 2009;21:76–81.
OCTOBER 2014–VOL. 62, NO. 10
JAGS
EOSINOPHILIC COLITIS: A RARE CAUSE OF LOWER GASTROINTESTINAL BLEEDING IN AN ELDERLY ADULT To the Editor: Lower gastrointestinal bleeding (LGIB) affects a significant number of elderly adults and is an important cause of morbidity and mortality. The incidence of LGIB increases with age and is more common in men than women.1 Reviewing the literature, LGIB associated with eosinophilic colitis in an elderly adult has never been reported. Herein is presented a 77-year-old woman with LGIB due to eosinophilic colitis (EC) who was successfully treated with prednisone and azathioprine. The woman was admitted to the hospital with complaints of rectal bleeding and abdominal pain. She had a 20-year history of hypertension. Laboratory findings were serum hemoglobin 6.7 g/dL, white cell count 12,500/lL with 20% eosinophils (eosinophil count 2,500/lL) and platelet count 240,000/lL. Biochemical tests were within normal limits. History revealed no allergic disease, food or drug allergy, or use of antibiotics. Physical examination was unremarkable except for diffuse abdominal tenderness. Colonoscopy showed two rectal ulcers 22 and 12 mm in diameter. Multiple biopsies were taken (Figure 1). Histopathological examination of rectal ulcers showed active inflammatory reaction with focal clusters of eosinophils in lamina propria consistent with EC. Prednisone 40 mg/d and azathioprine 100 mg/d were started, and her symptoms, including rectal bleeding and abdominal pain, resolved within 2 weeks. Four weeks after discharge from the hospital, colonoscopy was normal and she no longer had any symptoms. EC is a rare clinical condition that most frequently affects neonates and young adults. Clinical presentation of EC is usually nonspecific and depends on the layer of intestinal wall that eosinophils have infiltrated. Abdominal pain, nonbloody and bloody diarrhea, and significant weight loss are the hallmarks of EC.2 EC may also present acutely and lead to severe and fatal complications such as hemorrhage and perforation.3 Two neonates with LGIB due to EC have been reported in the literature. The authors suggested that infiltrated eosinophils in the colonic mucosa could be involved in the pathogenesis of LGIB.4
Figure 1. Colonoscopic examination revealed the white base of a 12-mm-long rectal ulcer (black arrow).
JAGS
OCTOBER 2014–VOL. 62, NO. 10
Eosinophilic colitis is a rare clinical condition, so the most important factor in making the diagnosis is to have a high degree of clinical suspicion. In conclusion, clinicians should consider EC in the differential diagnosis of LGIB in elderly adults, and early medical treatment should be initiated to avoid serious complications. G€ ulay Kocßak, MD Department of Nephrology, C ß anakkale Onsekiz Mart University, C ß anakkale, Turkey Erdem Kocßak, MD Department of Gastroenterology, C ß anakkale State Hospital, C ß anakkale, Turkey Erdem Akbal, MD Department of Gastroenterology, C ß anakkale Onsekiz Mart University, C ß anakkale, Turkey Hacer Sßen, MD G€ okhan Erba g, MD Ceren Erdo gan, MD Department of Internal Medicine, C ß anakkale Onsekiz Mart University, C ß anakkale, Turkey
ACKNOWLEDGMENTS Conflict of Interest: The editor in chief has reviewed the conflict of interest checklist provided by the authors and has determined that the authors have no financial or any other kind of personal conflicts with this paper. Author Contributions: G€ ulay Kocßak: manuscript concept and design. Erdem Kocßak, G€ okhan Erba g: preparation of manuscript. Erdem Akbal, Hacer Sßen: analysis and interpretation of data. Ceren Erdo gan: subject’s doctor. Sponsor’s Role: No sponsor associated with manuscript.
REFERENCES 1. Chait MM. Lower gastrointestinal bleeding in the elderly. World J Gastrointest Endosc 2010;2:147–154. 2. Alfadda AA, Schaffer EA, Urbanski SJ et al. Eosinophilic colitis is a sporadic self-limited disease of middle-aged people: A population-based study. Colorectal Dis 2014;16:123–129. 3. Yeo SA, Lim YK, Lim KH et al. Toxic haemorrhagic colitis: A rare presentation of eosinophilic colitis. Case Rep Gastrointest Med 2012;2012: 279813. 4. Ohtsuka Y, Shimizu T, Shoji H et al. Neonatal transient eosinophilic colitis causes lower gastrointestinal bleeding in early infancy. J Pediatr Gastroenterol Nutr 2007;44:501–505.
CASE REPORT: SENILE-ONSET AMYLOIDOSIS PRESENTING WITH PAINFUL LOWER EXTREMITY NEUROPATHY To the Editor: Peripheral neuropathy symptomatology ranges from intermittent numbness to constant burning with muscle weakness. Neuropathy interferes with postural control and is a risk factor for falls1 in community-dwelling elderly adults. Identifying the etiology of peripheral neuropathy in elderly adults is challenging because they often have multiple comorbid conditions that may
LETTERS TO THE EDITOR
2017
contribute to the development of this disorder. Pinpointing the cause, such as in senile-onset amyloidosis, whose incidence in elderly adults is unknown and whose prevalence increases with age (seen in 25% of 80-year-olds),2 can help prevent further nerve damage, disability, and falls and help clinicians inform people on their likely prognosis. A high-functioning 73-year-old man presented for an initial geriatric consultation complaining of 12-year progressive lower extremity neuropathic pain accompanied by weakness and imbalance. He had undergone multiple evaluations and was comanaged by staff in a pain clinic using pharmacological and nonpharmacological approaches with the working diagnosis of idiopathic peripheral sensory neuropathy with paresthesias for longer than 5 years. He also complained of dyspnea on exertion for a few months without chest pain or palpitations. His medical history included diabetes mellitus, hypothyroidism, coronary artery disease (CAD), previous myocardial infarction, pacemaker placement, anterior cervical fusion, and bilateral carpal tunnel release in 1998 and 2003. The man was married and employed as a college football coach. He was independent in basic and instrumental activities of daily living. He had a family history of early CAD in his father and brother. On physical examination, his lower extremities had 1+ edema, diminished sensation to monofilament, diminished vibratory sense, dystrophic toenails, palpable pulses, no gross deformity, and intact skin. Cranial nerves were intact, with normal tone, bulk, and strength in his extremities. Reflexes were 1+ except 0 at the Achilles tendon. Romberg was positive. His gait was wide-based and ataxic on tandem walking. His heart rate and rhythm were regular without a third heart sound, and his jugular venous distention was measured at 12 cm. Cognitive testing was normal. Laboratory testing revealed serum protein electrophoresis with no M-protein, a urine protein electrophoresis with trace proteinuria, and free light chains with free kappa of 23.7 and free lambda of 22.6 with a normal K/L ratio. Bone marrow biopsy was negative. Nerve conduction study in 2001 revealed mild demyelination and axonopathy. Subsequent studies, in 2008 and 2012, revealed dramatic progression of a severe sensorimotor axonopathy with demyelinating features and absent lower extremity sensory nerve action potentials (SNAPs). An echocardiogram showed thickening of the left ventricular wall and worsening diastolic filling consistent with restriction. Electrocardiograms revealed low-voltage QRS complexes from 2005 to 2012. He underwent cardiac muscle biopsy, which revealed amorphous eosinophilic deposition that Congo red staining confirmed to be amyloid. Because immunostains for classification of subtypes were unrevealing, further subtype investigation was undertaken with transthyretin (TTR) genetic analysis.
DISCUSSION Amyloidosis results from protein misfolding and deposition within tissues. As a result, neuropathy often presents as a progressive, symmetric, axonal disease of the distal lower extremities with prominent small fiber features, ultimately affecting motor and sensory fibers, decreased SNAPs, and relatively normal conduction velocities.3 The cause of
