Response to Hypoglycemia an Enigmatic Dilemma.34 Southern Medical Journal

8/13/2019 Response to Hypoglycemia an Enigmatic Dilemma.34 Southern Medical Journal

1/10

Letters to the Editor

Letters to the Editor are welcomed. They

may report new clinical or laboratory

observations and new developments in

medical care or may contain comments

on recent contents of the Journal. They

will be published, if found suitable, as

space permits. Like other material sub-

mitted for publication, letters must be

typewritten, double-spaced, and must not

exceed two typewritten pages in length.

No more than five references and one

figure or table may be used. See Infor-

mation for Authors for format of refer-

ences, tables, and figures. Editing, possi-

ble abridgment, and acceptance remain

the prerogative of the Editors.

Breast Cancer Metastasisto the GasserianGanglion

To the Editor: In an autopsy study of

309 patients with breast carcinoma me-

tastases to the central nervous system,

the brain was most frequently affected,

followed by the meninges and the spi-

nal cord.1 In this letter, we describe a

patient with breast cancer who had met-

astatic tumor in the gasserian ganglion.A 37-year-old woman came to her

oncologist with numbness on the right

side of her face of 1 months duration.

Several years before, she underwent

right modified radical mastectomy fol-

lowed by adjuvant chemotherapy and

locoregional radiotherapy for stage IIIA

breast cancer. More than 1 year later,

she was treated by radiation for pallia-

tion of symptomatic osseous metastatic

disease in the spine.

On physical examination, sensa-tion was significantly impaired in all

three divisions of the fifth cranial nerve

on the right side.

The presence of metastatic neo-

plasm in the gasserian ganglion area

(right side) of the skull base was dem-

onstrated (Fig. 1, A andB) by MRI.

After intracranial clivus metastasis

was diagnosed, 4 mg dexamethasone (3

times daily p.o.) and local irradiation

was started. After completion of radio-

therapy (30 Gy/10 fractions), there was

some degree of improvement of the

hemifacial sensory dysfunction. The pa-

tient died of her illness 5 months later.

In a report of 10 patients with breast

cancer with metastatic tumor causing cra-

nial nerve palsies in the absence of intra-

cranial tumor, Hall et al2 found extensive

disease at the skull base compressing the

nerves; there was no instance of trigem-

inal ganglion involvement.

Metastatic tumor involving the gas-

Sagittal (A) and coronal (B) postcontrast T1-weightedMRI show an enhancing right gasserian ganglion mass(arrows).

Southern Medical Journal Volume 99, Number 1, January 2006 93


2/10

serian ganglion was reported by Power

in 1886 and then by Parves-Stuart in

1927.3 Iniguez et al4 described a case

of neuropathy of the chin as the pre-

senting symptom of breast cancer; the

manifestation was explained on the ba-

sis of a metastatic lesion in the trigem-inal ganglion shown on MRI as enlarge-

ment of the gasserian ganglion (an

exhibited abnormality akin to that of

our patient). Other reported manifesta-

tions of the secondary affliction are par-

esthesia of the mental and infraorbital

regions or unilateral decreased sensa-

tion to pinprick in all three divisions of

the fifth cranial nerve.

Radiotherapy is the treatment of

choice for skull base metastases be-

cause it is effective in achieving palli-ation5 (such therapy was partly success-

ful in our case). The role of surgery or

chemotherapy for this special disease

condition is not well established.

In conclusion, the trigeminal gan-

glion is a rare site of metastasis. On-

cologists should have a heightened

awareness of the unpredictable behav-

ior of carcinoma of the breast, particu-

larly in terms of body locations of neo-

plastic spread. This example represents

only the second case known to us to bereported in the English literature. Thus,

definitive conclusions concerning ther-

apeutic management and prognosis

have not been ascertained. The unique

occurrence of metastatic tumor in the

gasserian ganglion was a preterminal

event in our patient.

Federico L. Ampil, MD

Gary V. Burton, MD

Mardjohan Hardjasudarma, MD

Travis Henley, MD

Departments of Radiology and MedicineLouisiana State University HealthSciences CenterShreveport, LA

References1. Tsukada Y, Fouad A, Pickren JW, et al. Cen-

tral nervous system metastases from breastcarcinoma: autopsy study. Cancer 1983;52:23492354.

2. Hall SM, Buzdar AU, Blumenschein GR. Cra-

nial nerve palsies in metastatic breast cancer

due to osseous metastasis without intracranial

involvement.Cancer1983;52:180184.

3. Willis RA. The spread of tumours in the hu-

man body. St. Louis, CV Mosby, 1952, p. 257.

4. Iniguez C, Mauri JA, Larrode P, et al. Mandib-

ular neuropathy due to infiltration of the gasse-

rian ganglion. Rev Neurol1997;25:10921094.

5. Greenberg HS, Deck MDF, Vikram B, et al.

Metastases to the base of skull: clinical find-ings in 43 patients. Neurology 1981;31:530

537.

Hyperglycemia in anElderly Diabetic Patient:Drug-drug or Drug-disease Interaction?

To the Editor:The use of gatifloxacin

is increasing as the result of convenientdosing and efficacy in a wide range of

infectious diseases. Gatifloxacin is gen-

erally well tolerated; however, recently

there have been several reports of al-

terations in glucose levels in patients

receiving gatifloxacin.

An 80-year-old male with a medi-

cal history significant for type 2 diabe-

tes mellitus, hypertension, coronary ar-

tery disease, hypothyroidism, and

benign prostatic hypertrophy presented

to the emergency room (ER) with acomplaint of elevated blood sugar.

Medications included 2.5 mg glipizide,

400 mg gatifloxacin, 25 mg metopro-

lol, aspirin, 0.075 mg levothyroxine, 10

mg felodipine, 5 mg finasteride, 20 mg

omeprazole, and 25 mg hydrochlorothi-

azide.

He was discharged from the hos-

pital 10 days previously after a 3-day

inpatient stay for pneumonia. Initial an-

tibiotic therapy was ceftriaxone and

azithromycin that was changed to 400mg gatifloxacin p.o. daily at discharge.

During his hospitalization, his random

blood glucose ranged from 93 mg/dL to

152 mg/dL. His most recent HgbA1c 2

months before admission was 5.4%.

One day before this presentation he no-

ticed lightheadedness, and he found that

his glucose was elevated. His glucose

in the ER was 510 mg/dL. Other labo-

ratory values of note were a blood urea

nitrogen level of 35 mg/dL and a serum

creatinine level of 2.1 mg/dL. He was

treated with intravenous fluids, subcu-

taneous regular insulin, and discharged

with instructions to complete the course

of gatifloxacin at a reduced dose of 200

mg p.o. daily. He continued to have el-

evated blood sugar at home and he re-

turned to the ER 2 days after being re-

leased. His glucose level at this visit

was 516 mg/dL. On examination, a tem-

perature of 97.9, a pulse of 78 beats

per minute, a respiratory rate of 16

breaths per minute, blood pressure of

117/62 mm Hg, and a normal physical

examination were noted. The patient re-

ported no change in any of his medica-

tions other than gatifloxacin, and there

was no noticeable change in diet or ex-ercise. He was treated with intravenous

fluids and subcutaneous regular insulin,

and the gatifloxacin was stopped. With

this modification, his repeat random

blood glucose levels were 488 mg/dL,

260 mg/dL, and 187 mg/dL on three

occasions over the next week.

Gatifloxacin has a broad spectrum

of activity, with a wide range of clinical

utility. A few case reports indicate that

both hypoglycemia and hyperglycemia

can be associated with this agent.14 Inour case, decreased creatinine clearance

along with higher doses of gatifloxacin

might have contributed to the accumu-

lation of the drug, with worsening of

hyperglycemia. The mechanism of hy-

perglycemia associated with gatifloxa-

cin is currently unknown. The relation-

ship of gatifloxacin and glucose control

supports gatifloxacin as the cause, as

does the improvement in glucose con-

trol after gatifloxacin therapy was dis-

continued. The Naranjo probability

scale suggests a possible drug-related

event.5

In conclusion, gatifloxacin therapy

may precipitate severe hyperglycemia

in patients with diabetes, especially in

the elderly population. Awareness of

this complication will allow us to an-

ticipate and prevent hyperglycemia.

Clinicians should educate their dia-

betic patients to this possible side ef-


94 2006 Southern Medical Association


3/10


4/10

References1. Parhami F, Tintut Y, Beamer WG, et al.

Atherogenic high fat diet reduces bone min-eralization in mice. J Bone MineralRes 2001;16:182188.

2. Chan MH, Mak TW, Chiu RW, et al. Simvasta-

tin increases serum osteocalcin concentration in

patients treated for hypercholesterolaemia. J

Clin Endocrinol Metab 2001;86:45564559.

3. Yamaguchi T, Sugimoto T, Yano S, et al.

Plasma lipids and osteoporosis in postmeno-

pausal women. Endocr J2002;49:211217.

4. Tanko LB, Nielsen SB, Christiansen C. Does se-

rum cholesterolcontribute to vertebral bone loss in

postmenopausal women?Bone 2003;32:814.

5. Poli A, Bruschi F, Cesana B, et al. Plasma

low-density lipoprotein cholesterol and bone

mass densitometry in postmenopausal women.

Obstet Gynecol2003;102:922926.

Response toHypoglycemiaAnEnigmatic Dilemma

I agree with Dr. Ranjodh Gill, author of

the editorial published in the July 2005

issue of the Southern Medical Journal

entitled HypoglycemiaAn Enig-

matic Dilemma, that for best diag-

nostic yield, patients should undergo

testing during an episode of spontane-

ous hypoglycemia.1 In addition, I con-tend that this includes taking simulta-

neous blood samples not just for insulin

levels, but also for cortisol levels, in

light of the fact that spontaneous hypo-

glycemia may be a presenting feature

of secondary hypoadrenalism.2

O. M. P. Jolobe, MRCPManchester Medical Society

Manchester, United Kingdom

References1. Gill R. Hypoglycemia-an enigmatic dilemma.

South Med J2005;98:679.

2. Jolobe OMP, Htin TS. Hyponatraemia and

spontaneous hypoglycemia. Postgraduate

Medical Journal1997;73:675677.

Extreme Hyperkalemia

To the Editor:Hyporeninemic hypoal-

dosteronism was one of the postulated

mechanisms mediating hyperkalemia in

the case report by Dr. H. A. Tran pub-

lished in the July 2005 issue of the

Southern Medical Journal.1 I would add

that emergency treatment of intractable

hyperkalemia should include not only

routine measures such as calcium glu-

conate and insulin and glucose infusion,as mentioned by the author, but also

intravenous sodium bicarbonate and

-adrenergic agonists, the latter paren-

terally or by nebulization.2 There may

also be a place for empiric treatment

with parenteral hydrocortisone when

the biochemical profile is compatible

with hyporeninemic hypoaldosteronism

and risk factors for this condition are

present. This was the case in a patient

who was being treated with the heparin

analogue pentosan polysulfate in thepresence of nephrocalcinosis and in

whom hyperkalemia remained refrac-

tory, not only to intravenous calcium

gluconate, insulin, and glucose, but also

to the cation exchange resin calcium

resonium. Only on the fourteenth day,

when she was coprescribed intravenous

hydrocortisone, sodium bicarbonate in-

fusion, and nebulized albuterol, did her

plasma potassium fall from 7.2 mmol/L

to 3.4 mmol/L.3 Arguably, the thera-

peutic contribution of hydrocortisonewas attributable to its mineralocorticoid

action, given the fact that mineralocor-

ticoids ameliorate hyperkalemia in hy-

poreninemic hypoaldosteronism.4,5

O. M. P. Jolobe, MRCPManchester Medical Society

Manchester, United Kingdom

References1. Tran HA. Extreme hyperkalemia.South Med J

2005;98:729732.

2. Singer GS, Brenner BM. Fluid and electrolytedisturbances. In Fauci AS, Braunwald E, Is-

selbacher KJ, Wilson JD, Martin JB, Kasper

DL, Hauser SL, Longo DL (eds): Harrisons

Principles of Internal Medicine Chapter 49,

14th ed, McGraw-Hill Health Profession Di-

vision, New York, 1998.

3. Jolobe OMP. Hyperkalaemic paralysis (letter).Age Ageing2003;32:556557.

4. Orth DN, Kovacs WJ. The Adrenal Cortex. In

Wilson JD, Foster DW, Kronenberg HM,

Larsen PR (eds): Williams Textbook of Endo-

crinology, 9th ed, WB Saunders Co, Philadel-

phia, 1998.

5. De Fronzo RA. Hyperkalemia and hyporenine-

mic hypoaldosteronism. Kidney Int1980;17:

118134.

Primary SternalOsteomyelitis Caused ByActinomyces israelii

To the Editor: Primary sternal osteo-

myelitis (PSO) is a rare entity. Diagno-

sis is usually difficult due to the non-

specific clinical picture and late

radiological findings. We describe a

case of PSO due to Actinomyces israe-

lii and how ultrasonography (US), CT,

and MRI helped to make the diagnosis

and guide treatment.A previously healthy 50-year-old

woman without history of trauma pre-

sented with painful presternal swelling

and fever. A 5-cm warm, fluctuating

mass overlying the sternal manubrium

was palpated. There was leukocytosis

with neutrophilia. Blood cultures were

sterile. A chest x-ray was normal. On

US, thickening of the insertion of the

right pectoralis major muscle on the ma-

nubrium, an adjacent heterogenous hy-

poechoic collection, and irregularitiesof the contour of the sternum were de-

tected. An US-guided aspiration yielded

purulent material. A contrast-enhanced

CT demonstrated hypodense soft-tissue

swelling, with enhancement surround-

ing the sternum and right chondroster-

nal joint. She was unresponsive to clox-

acillin and surgical debridement. A

MRI showed an extensive involvement

of the sternal manubrium with de-

creased signal intensity on T1-weighted

images (T1-WI) and increased signalon T2-WI of the bone marrow, progres-

sion of the cortical erosions involving

the anterior and posterior aspects of the

sternum, and the 2nd4th chondroster-

nal joints, with associated pleural thick-

ening. Right pectoralis major muscle

and peristernal soft tissues appeared

thickened and hypointense on T1-WI

(Fig. 1). Culture of the bony material

yieldedA israelii.

She was treated with IV penicillin




5/10

G and extensive surgical debridement,

guided by MRI findings, leading to

quick disappearance of the fever and

improvement of the presternal swelling.

Dental caries and periodontal disease

of the first and second molar teeth bi-laterally were identified. These teeth

were removed, and anaerobic bacteria,

but not A israelii, were isolated. On the

sixth week of treatment she was dis-

charged afebrile on oral antibiotherapy.

Most cases of sternal osteomyelitis

are complications of sternotomy or tho-

racic trauma, and less frequently are

secondary to spread from contiguous

foci.1 PSO is caused by hematogenous

dissemination, usually in the setting of

IV drug abuse or immunosuppression.Most cases of PSO are caused by Staph-

ylococcus aureus, Gram negative bacte-

ria, Candida, and Aspergillus sp.2 Acti-

nomycessp are Gram positive anaerobic

bacteria found in the normal oral flora

which are involved in oral-cervicofacial

infections. They have seldom been re-

ported as the cause of osteomyelitis of

the facial bones.3 Periodontal disease,

damage to mucosal barriers, aspiration,

and immunosuppression are risk factors.

A breach in the oral mucosa leads to its

introduction into the soft tissues, from

where it may spread to the facial bones in

a contiguous fashion. In our patient the

presumptive portal of entry forA israelii

was oral and an ulterior hematogenousseeding probably caused the sternal in-

fection. The ongoing penicillin treatment,

together with the difficulties inherent to

the culture ofActinomycesmay have pre-

vented its isolation from the teeth.

Diagnosis of sternal osteomyelitis

is straightforward in cases secondary to

sternotomy or trauma and bone destruc-

tion on x-rays. However, PSO is often

difficult to diagnose due to the nonspe-

cific symptoms and late radiological

changes. Plain film findings, which lag

1 to 2 weeks, include increased density,

displacement of soft tissues, and bone

loss.1,2 Technetium-99 scintigraphy is

positive earlier and has a good sensi-

tivity, but lacks specificity.4 Despite the

limitations of US in the assessment of

bone, in our case, the irregularities of

the sternal contour and the inflamma-

tory changes of the muscles raised sus-

picion of osteomyelitis and prompted

further evaluation. CT may show a

peristernal soft-tissue mass, periostitis,

and bone destruction. But occasionally,

it may be difficult to distinguish inflam-

matory soft-tissue infection with reac-

tive periostitis from true PSO. In such

cases, MRI provides better visualiza-

tion of soft-tissue planes and inflamma-

tory changes in the bone, an excellent

resolution, and multiplanar capacity

that allow precise delineation of the ex-

tent of soft tissue and osseous involve-

ment, which are invaluable in the pre-

surgical assessment.4 In our patient,

MRI showed a more extensive osseous

and soft-tissue involvement, pleural

thickening, excluded mediastinum in-

volvement, and enabled surgeons to tai-lor surgical therapy and achieve a com-

plete debridement.

A prompt diagnosis of PSO is essen-

tial for appropriate treatment and to avoid

extension to the mediastinum. US may

have a role in the assessment of sternal

abnormalities, and provides an accessible

means of obtaining tissue samples. Both

CT and MRI are extremely useful in the

diagnosis, but we favor MRI as the

method of choice for assessing its exten-

sion and for surgical planning.I. Pinilla, MD, PhD

C. Martn-Hervas, MD, PhD

E. Gil-Garay, MD, PhD

Departments of Radiology andOrthopedic Surgery

Hospital Universitario La PazMadrid, Spain

References1. Franquet T, Gimenez A, Alegret X, et al. Im-

aging findings of sternal abnormalities. Eur-Radiol1997;7:492497.

2. Lin JC, Miller SR, Gazzaniga AB. Primary

sternal osteomyelitis. Ann Thorac Surg1996;

61:225227.

3. Yenson A, deFries HO, Deeb ZE. Actinomy-

cotic osteomyelitis of the facial bones and

mandible.Otolaryngol Head Neck Surg1983;

91:173176.

4. Moylett E, Chung T, Baker C. Magnetic res-

onance imaging in a child with primary sternal

osteomyelitis. Pediatr Infect Dis J 2001;20:

547550.

Fig. Sagittal T1-weighted MR image reveals extensive involve-ment of the sternal manubrium with decreased bone marrow

signal intensity and cortical erosions involving the anterior and

posterior aspects of the manubrium. There is a hypointense

soft-tissue swelling in the pre- and retrosternal regions, as well

as pleural thickening.




6/10

Distribution of PleuralEffusion in CongestiveHeart Failure

To the Editor: The recent article by

Woodring questioned the classicstatement of predominantly right-

sided pleural effusions in patients

with congestive heart failure (CHF),

on the basis of a study of 120 patients

whose cardiac pleural effusions were

equally distributed between the right

and the left hemithorax.1 More im-

portantly, the author also concluded

that left-sided effusion is not an atyp-

ical finding in CHF and is not, in and

of itself, an indication for further clin-

ical or imaging workup to find alter-native causes. This latter point seems

to contradict Lights recommenda-

tions2 and consensus guidelines,3 and

may possibly influence practice

trends. Therefore, we present our own

experience with the radiographic dis-

tribution of cardiac pleural effusions

in the largest clinical series to our

knowledge.

In the last 12 years, we identified

221 of 1,515 consecutive patients who

underwent diagnostic thoracentesis ashaving CHF, at the University Hospital

Arnau de Vilanova (Lleida, Spain). The

diagnosis of CHF was established by

clinical criteria (presentation, pleural

fluid characteristics, and response to

therapy). Twenty-four patients were ex-

cluded from the analysis because pos-

teroanterior chest x-rays were not per-

formed or available. The final analysis

group of 197 patients consisted of 98

(50%) males and 99 (50%) females,

with a mean age of 77 9 years. As

shown in the Table, we found a statis-

tically significant difference in the dis-

tribution of pleural effusion between the

right and left hemithorax (102 versus

39,2 27.26,P 0.001), even when

considering only unilateral effusions

(62 versus 18, 2 24.20,P 0.001).

Seventy-seven percent of patients had

effusions that occupied a third or less

of the hemithorax in the posteroanterior

radiographic view. When four clinical

series comprising 441 patients with

CHF are combined,1,4,5

304 (69%) pa-tients had bilateral pleural effusions, 95

(21%) had unilateral right-sided effu-

sions, and 42 (9%) had unilateral left-

sided effusions (Table). However, ra-

diographic identification of pleural

effusion is insensitive and detects only

moderate to large amounts of pleural

fluid. In a study of 60 patients with de-

compensated CHF, chest CT was used

as the gold standard for the presence or

absence of pleural effusion.6 As many

as 52 (97%) of the 60 patients had pleu-ral effusion; of these, 23 (44%) had

equally bilateral effusion, 20 (38%) had

right-sided predominant bilateral effu-

sion, 2 (4%) had left-sided predominant

bilateral effusion, 5 (10%) had right-

sided effusion only, and 2 (4%) had left-

sided effusion only. Again, 2 analysis

shows a statistically significant differ-

ence between the right and left hemi-

thorax (25 versus 4, 2 15.20, P

0.001).

To conclude, pooled data demon-

strate a great preponderance of bilateral

pleural effusions in CHF, and approxi-mately double numbers of unilateral

pleural effusions on the right side than

on the left. For this reason, contrary to

the suggestion of Woodring, we think

that in the context of CHF thoracentesis

is indicated if more than a minimal uni-

lateral effusion (particularly left-sided)

exists. Acting on Woodrings advice

may provide clinicians false reassur-

ance when evaluating patients with uni-

lateral left-sided effusions in the setting

of heart disease, thus missing importantcauses of exudative pleural effusions

such as pericardial disease, postcardiac

injury syndrome or postcoronary artery

bypass surgery, as well as comorbid

conditions such as pulmonary embo-

lism or pneumonia.

Jose M. Porcel, MDDepartment of Internal Medicine

Arnau de Vilanova University HospitalLleida, Spain

Manuel Vives, MD

Division of Internal MedicineClnica Recoletas

Albacete, Spain

References1. Woodring JH. Distribution of pleural effusion

in congestive heart failure: what is atypical?South Med J2005;98:518523.

Table. Published series on the distribution of cardiac pleural effusions assessed by chest radiography a

Currentseries Woodring,20051

Peterman and

Brothers,19834 Sum ofprevious seriesb

Weiss and

Spodick,19845 Sum of allseriesc

Right 62 (31) 18 (15) 2 (4) 82 (22) 13 (19) 95 (21)

Left 18 (9) 15 (12,5) 3 (5,5) 36 (10) 6 (9) 42 (9)

Bilateral R L 40 (20) 25 (21) 16 (30) 81 (22)

Bilateral R L 56 (28) 36 (30) 19 (35) 111 (30) 51 (73) 304 (69)

Bilateral L R 21 (11) 26 (22) 14 (26) 61 (16)

Total 197 120 54 371 70 441

aData are presented as No. (%). R right; L left.bDifference between the right and left side is significant (163 vs 97, 2 16.75, P0.001).cDifference between unilateral right and left side is significant (95 vs 42, 2 20.5, P0.001).




7/10

2. Light RW. Pleural effusion. N Engl J Med

2002;346:19711977.

3. Maskell NA, Butland RJ, Pleural Diseases

Group, Standards of Care Committee, British

Thoracic Society. BTS guidelines for the in-

vestigation of a unilateral pleural effusion in

adults. Thorax 2003;58 (Suppl 2):ii817.

4. Peterman TA, Brothers SK. Pleural effu-sions in congestive heart failure and in

peric ardia l dise ase. N Engl J Med 1983;

309:313.

5. Weiss JM, Spodick DH. Laterality of pleural

effusions in chronic heart failure. Am J Car-

diol1984;53:951.

6. Kataoka H. Pericardial and pleural effusions

in decompensated chronic heart failure. A m

Heart J 2000;139:918923.

Localized Amyloidosis of

Cardiac and SkeletalMuscle: InvestigatePromptly Where ItManifests

To the Editor:A negative biopsy may

not rule out amyloidosis, as seen in the

following case. We report the case of a

patient with cardiac and muscular man-

ifestations of amyloidosis, who had a

normal rectal mucosal biopsy. The di-

agnosis of amyloidosis was only estab-lished at autopsy.

A 58-year-old male was admitted

with pulmonary edema. He had experi-

enced lower limb weakness, muscle

cramps, and easy fatigability for 2.5

years, and had a 6 month history of

shortness of breath. In addition, he had

a history of arterial hypertension and

was a previous smoker. Clinical exam-

ination revealed pulmonary rales and

leg edema. Electrocardiography

showed Q-waves in the posterolateralleads. Chest x-ray revealed pulmonary

congestion. Troponin-T (semiquantita-

tively) and creatine kinase (188 U/L,

normal 80 U/L) were elevated. Cor-

onary angiography revealed a 90% ste-

nosis of the left anterior descending ar-

tery. Echocardiography (Fig.) showed a

thickened, echodense left ventricular

myocardium (13 mm, normal 11

mm) and an enlarged left atrium (43

mm, normal 40 mm). Systolic func-

tion was normal (fractional shortening

25%), but pulsed wave Doppler sonog-

raphy of the transmitral flow showed a

deceleration time of less than 150 mil-

liseconds and an E-velocity of 1.16 m/s

with an E/A ratio 2, indicating re-

strictive cardiomyopathy. Dipyridamolstress echocardiography revealed re-

versible hypokinesis of the midseptal

and apicoseptal segments, and coronary

bypass grafting was considered. The pa-

tient was discharged with acetylsali-

cylic acid, metoprolol and ramipril. The

patients restrictive cardiomyopathy

was suspected to be due to amyloidosis

since there were no indications for en-

domyocardial fibrosis, sarcoidosis,

hemochromatosis, Fabry or Gaucher

disease, Hurler syndrome, or glycogenstorage disease. Bone marrow aspira-

tion revealed 20% plasma cells. Immu-

nohistochemistry exhibited a domi-

nance of-positive plasma cells, but no

evidence of clonal light-chain restric-

tion, being confirmed by a polyclonal

pattern of immunoglobulin gene rear-

rangement on polymerase chain reac-

tion for the VDJ heavy chain locus.

Due to complaints of dizziness,

muscle pain in the limbs, weakness of

the upper eyelids and chewing musclesafter physical stress, as well as worsen-

ing heart failure, the patient was read-

mitted after 10 weeks. Clinical exami-

nation revealed massive peripheral

edema, dyspnea, and a weight gain of 8

kg. Creatinine was 1.6 mg/dL (normal

1.1 mg/dL) and creatine-kinase was

repeatedly elevated (80103 U/L, nor-

mal 80 U/L). Serum troponin-T was

normal. Brain natriuretic peptide was

11,070 pg/mL (normal 227 pg/mL).

Fractional shortening had deterioratedto 15% (normal 24%). Systolic blood

pressure was 80 mm Hg. Rectal biopsy,

light chains, and Bence-Jones protein

were negative. Considering the bone

marrow findings, immunologic and mo-

lecular biologic results, and the lack of

serologic evidence of gammopathy,

plasmacytosis was assumed reactive.

Clinical neurologic examination re-

vealed postural tremor, exaggerated

tendon reflexes on the lower limbs and

positive Babinski sign. Nerve conduc-

tion studies of the left median nerve

revealed slightly reduced amplitude of

the compound muscle action potential

on distal and proximal superficial stim-

ulation. Repetitive stimulation of the

left median nerve was normal. Acetyl-choline receptor antibodies were nor-

mal. Needle electromyography of the

right rectus femoral muscle revealed

shortened mean motor unit action po-

tential duration. Myopathy and poly-

neuropathy were suspected and a muscle

biopsy was performed. Two days before

the muscle biopsy, however, the patient

died suddenly at home. Autopsy, con-

fined to histologic examination of the

myocardium, showed interstitial deposi-

tion of Congo red positive material sub-endocardially and in the intramyocardial

artery walls. Immunohistochemistry re-

vealed a positive staining for antibodies

against amyloid P, absent staining with

antibodies against amyloid A and no re-

action with antibodies against kappa or

lambda chains. Due to autolysis, the

amyloid could not be further investi-

gated. The patients sister, children, and

nephews had normal clinical cardiologi-

cal examinations, electrocardiographies,

and echocardiographies.Amyloidosis may be acquired or

hereditary, localized, or systemic.1,2

Most likely the patient suffered from

either primary systemic (AL)-amyloid-

osis or from senile amyloidosis. Rapid

progression of the disease, however, fa-

vors AL-amyloidosis.2 History and in-

vestigations of the relatives excluded

familial amyloidosis. Chronic infection

was excluded by history and instrumen-

tal investigations. Cardiac involvement

occurs frequently in AL, hereditary, andsenile amyloidosis.3 Deposition of amy-

loid in the myocardial interstitial space,

vessel walls, valves, and conduction

system may lead to myocardial thick-

ening, coronary stenosis, valve abnor-

malities, arrhythmias, and diastolic dys-

function.1,4 A restrictive filling pattern

predicts poor outcome.1 It remains un-

certain, however, whether the coronary

stenosis was due to amyloidosis or ar-

teriosclerosis and whether the patients




8/10

sudden death was due to myocardial

ischemia or conduction system affec-

tion.4

In our patient, amyloidosis was

missed due to the fact that no clinically

affected organs were biopsied. (Rectal

biopsy in AL-amyloidosis is positive in

only 60 89% of cases.) In addition,

skeletal muscle affection was neglected,and diagnostic management was too

slow, facing the rapid progression and

poor outcome of the disease.1 The pa-

tient might have profited from heart

transplantation if amyloidosis had been

detected earlier. As soon as cardiac

amyloidosis is suspected, prompt diag-

nosis is essential.

Claudia Stollberger, MD

Christina Steger, MD

Marion Avanzini, MDSecond Medical Department

Krankenanstalt RudolfstiftungVienna, Osterreich

Hans Feichtinger, MDDepartment of Pathology

Krankenanstalt RudolfstiftungVienna, Osterreich

Robert Ullrich, MDDepartment of Pathology

Allgemeines KrankenhausVienna, Osterreich

Josef Finsterer, MDKrankenanstalt Rudolfstiftung

Vienna, Osterreich

References1. Falk RH, Comenzo RL, Skinner M. The sys-

temic amyloidosis. N Engl J Med1997;337:898909.

2. Kyle RA, Spittell PC, Gertz MA, et al. The

premortem recognition of systemic senile

amyloidosis with cardiac involvement. Am

J Med1996;101:395400.

3. Dubrey SW, Cha K, Simms RW, et al. Elec-

trocardiography and Doppler echocardiogra-

phy in secondary (AA) amyloidosis.Am J Car-

diol1996;77:313315.

4. Palladini G, Malamani G, Co F, et al. Holter

monitoring in AL amyloidosis: prognostic im-

plications. Pacing Clin Electrophysiol 2001;

24:12281233.

5. Mandl LA, Folkerth RD, Pick MA, et al. Amy-

loid myopathy masquerading as polymyositis.

J Rheumatol2000;27:949952.

Pedometer-measuredWalking and Risk Factorsfor Disease

To the Editor: Research documenting

the health benefits of exercise is convinc-

ing, but finding ways to encourage sed-

entary patients to become more active re-

mains a challenge. Adherence to

vigorous, structured exercise programs is

particularly low. One generally inactive

subgroup is older women, and postmeno-

pausal women who do exercise tend to

engage in moderate activity, specifically

walking. The goal of this investigation

was to document the relationship be-

tween daily walking volume (steps per

day measured by a pedometer) and se-

lected cardiovascular risk variables in

postmenopausal women.Eighty-eight postmenopausal women

between the ages of 50 and 75 years

volunteered for participation in this

institutional-review-boardapproved

study at the University of Tennessee.

Body composition was determined us-

ing a three-compartment model in

which bone mineral content (GE Med-

ical Systems, Lunar DPX-NT, Madison,

WI) and total body density (air displace-

ment plethysmography, Life Measure-

ment Inc., Concord, CA) were measured.A 10 mL blood sample was obtained in

the early morning hours when the subject

was in a fasted and rested state. Samples

were analyzed in a certified laboratory

for total cholesterol (TC), high density

lipoprotein cholesterol (HDL-C), low

density lipoprotein cholesterol (LDL-C),

triglycerides (Trig), C-reactive protein

(CRP), glucose (Glu), and hemoglobin

A1C (A1C). Subjects subsequently wore

a pedometer for 10 to 14 days, and an

average daily step count was determined.Pearson correlations were used to explore

the relationship between walking volume

and cardiovascular risk variables (SPSS

version 11 for Macintosh, Chicago, IL).

Partial correlation coefficients were cal-

culated to examine the relationship be-

tween walking volume and risk factors

while controlling for the effect of body

fat percentage (%BF). ANOVA was used

to compare the HDL-C values among in-

dividuals in different physical activity

categories.The average age, %BF, and body

mass index of participants was 61.0

5.8 years, 40.2 9.2%, and 27.8 5.9

kg/m2, respectively. Subjects ranged

from very inactive (1,300 steps per day)

to highly active (14,000 steps per day).

The correlation between daily steps and

%BF was 0.404 (P 0.001). Walk-

ing volume was significantly related to

HDL-C, TC to HDL-C ratio, and Trig

(see Table).

Fig. Echocardiographic recording of the pulsed-wave signal of the transmitral flow,showing a high E-wave with a short deceleratin time of 150 msec (arrow) and a very

small A-wave (asterisk

). These abnormalities are indicative of a restrictive filling pat-tern.




9/10

Percent BF was significantly cor-

related with TC to HDL-C ratio and

HDL-C (see Table). Glu was signifi-

cantly related to both %BF (r 0.217,

P 0.043) and steps (r0.289,P

0.006), but there was no relationship

between A1C and these variables. CRP

was significantly related to %BF (r

0.395, P 0.001) but not steps (r

0.106, P 0.324). After controlling

for %BF, daily steps remained signifi-

cantly related to HDL-C (r 0.247,

P 0.016), TC to HDL-C ratio (r

0.284,P 0.008), Trig (r0.239,

P 0.026), and Glu (r0.226,P

0.035). The most active women, aver-

aging approximately 8,000 steps per

day, had a HDL-C of 71.6 2.6 mg/dL. This was significantly higher (P

0.05) than the HDL-C of women who

walked approximately 5,000 steps per

day (56.6 2.7 mg/dL).

Walking is the most common phys-

ical activity chosen by women,1 and the

relationship between walking and health

outcomes is particularly strong in this

group.2,3 This study provides additional

evidence that daily walking is linked to

important cardiovascular risk variables.

Not surprisingly, these variables were

also strongly associated with %BF.

These data provide support for the im-

portant role that regular walking and

weight control play in promoting cardio-vascular health in postmenopausal

women.

Pedometer-monitored programs are

effective in helping sedentary individuals

become more active.4,5 This may be due

to the fact that pedometer-monitored pro-

grams use goal setting and self-monitor-

ing as reinforcement. There is evidence

that the addition of a pedometer to a brief

counseling session by a physician will

lead to greater daily walking.5 Given that

walking is a generally safe form of aer-obic exercise and yields important health

benefits, physicians might consider pre-

scribing pedometer-monitored programs

for inactive patients.

Dixie L. Thompson, PHD

Emily M. Krumm, MS

Olivera L. Dessieux, MS

Pamela Andrews, MSCenter for Physical Activity and Health

Department of Exercise, Sport, andLeisure Studies

University of TennesseeKnoxville, TN

References1. Rafferty AP, Reeves MJ, McGee HB, et al.

Physical activity patterns among walkers and

compliance with public health recommenda-

tions. Med Sci Sports Exerc 2002;34:1255

1261.

2. Thompson DL, Rakow J, Perdue SM. Rela-

tionship between accumulated walking and

body composition in middle-aged women.

Med Sci Sports Exerc2004;36:911914.

3. Manson JE, Greenland P, LaCroix AZ, et al.

Walking compared with vigorous exercise

for the prevention of cardiovascular eventsin women. N Eng J Med2002;347:716725.

4. Hultquist CN, Albright C, Thompson DL.

Comparison of walking recommendations in

previously inactive women. Med Sci Sports

Exerc2005;37:676683.

5. Stovitz SD, VanWormer JJ, Center BA, et al.

Pedometers and briefphysician counseling: in-

creasing physical activity for patients seen at a

family practice clinic. Med Sci Sports Exerc

2004;36:S241.

Table. Relationship between blood lipids and daily walking and body fat percentagea

TC HDL-C LDL-C TC/HDL-C Trig

Steps 0.122(0.256) 0.358(0.001) 0.188(0.079) 0.373(0.001) 0.285(0.007)

%BF 0.085(0.430) 0.338(0.001) 0.186(0.082) 0.314(0.003) 0.173(0.108)

Values represent Pearson correlation coefficients with the significance level in parentheses.aTC, total cholesterol; HDL-C, high density lipoprotein cholesterol; LDL-C, low density lipoprotein cholesterol; TC/HDL-C, the ratio of TC to HDL-C; Trig,triglycerides; Steps, average daily steps; % BF, body fat percentage.




10/10

Errata

In the December 2005 issue two authors names were misspelled. In the Table of Contents, the first author under

Religious Awareness Training for Medical Students: Effect on the Clinical Behavior should have read John T.

Chibnall. The author of the Selected Annotated Bibliography (South Med J2005;98:12511254) should have read

Conrad C. Daly, MTh. We regret these errors.

In Socolar RRS, Savage E, Keyes-Elstein L, et al. Factors that affected parental disciplinary practices of children

aged 12 to 19 months. South Med J2005;98:11811191, the following changes should have been made:

In Table 2 the following variables are given in percentages: Respondents relationship to child, Maternal race,

Paternal race, Maternal education, Cut off for CES-D, Knowledge of Infant Development, Boys, Householdincome, Maternal marital status, Number of people in household. Also, on the line that reads: Number of people in

household (N 167), there is a number 2 to the right of this phrase. This should not be there.

The last sentence of the first paragraph was not accurate. It should have read: In addition, the mode of administration,

including positive/negative demeanor, consistency, and follow-through, has not been studied.



Response to Hypoglycemia an Enigmatic Dilemma.34 Southern Medical Journal

Documents

Transcript of Response to Hypoglycemia an Enigmatic Dilemma.34 Southern Medical Journal