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Duke’s treadmill score in diabetics-does it really matter? Authors reply

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 418 Journal of Postgraduate Medicine October 2014 Vol 60 Issue 4

Letter to Editor

for prevention of postoperative infections in clean orthopaedic surgeries. Indian J Med Res 2013;137:111-6.

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Duke’s treadmill score in

diabetics-does it really

matter?

Sir,

This letter pertains to original article by Erkan, et al.[1] published in the recent issue. In this study authors attempted to correlate Duke’s treadmill score (DTS) with demographic and biochemical characteristics of enrolled subjects and statistically proved a positive correlation between DTS and serum HDL cholesterol levels. The patient population was classified in two groups as low and moderate to high risk according to Duke’s treadmill scores and both groups had no statistically significant difference in distribution of coronary artery disease (CAD) risk factors. I would like to draw your attention to distribution of diabetics in two groups with number far more, i.e. 19% in the low risk group versus 10.5% in the moderate to high risk group. This discrepancy in distribution of diabetics may not be merely by chance. It could well be that diabetics have lower DTS compared to non-diabetics for given CAD burden.[2] Long-term complications of diabetes in the form of diabetic neuropathy and nephropathy, physical deconditioning and obesity leads to inability to achieve maximum workload to induce ischemia and its related symptoms and ECG changes. Another potential reason may be that diabetic neuropathy causes decreased perception of angina, which is one of the variables in DTS.

Lakkireddy, et al.[3] in their study also observed that diabetics with moderate DTS had higher major cardiac event rates compared to non-diabetics. Thus, although DTS is a good score for post test cardiac risk stratification, with erroneous low scores, diabetic individuals may fall into the intermediate or low risk group and maybe wrongly managed conservatively.[4]

Lohiya RV

Department of Cardiology, Seth Gordhandas Sunderdas Medical College and King Edward Memorial Hospital, Mumbai, Maharashtra, India

Address for correspondence:

Dr. Rishi Vinod Lohiya, E-mail: rishidr123@rediffmail.com

References

1. Erkan AF, Ekici B, Demir GG, Töre HF. Lower levels of serum high-density lipoprotein cholesterol are associated with a worse Duke treadmill score in men but not in women. J Postgrad Med 2014;60:260-4.

2. Shaw LJ, Peterson ED, Shaw LK, Kesler KL, DeLong ER, Harrell FE Jr, et al. Use of a prognostic treadmill score in identifying diagnostic coronary disease subgroups. Circulation 1998;98: 1622-30.

3. La k k i r e d d y D R , B h a k k a d J, Ko r l a k u n t a H L , Ry s c h o n K, Shen X, Mooss AN, et al. Prognostic value of the Duke Treadmill Score in diabetic patients. Am Heart J 2005;150: 516-21.

4. George DH, Russell DW. Exercise stress testing in patients with type 2 diabetes: When are asymptomatic patients screened? Clin Diabetes 2007;25:126-30.

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www.jpgmonline.com DOI: 10.4103/0022-3859.143994 PubMed ID: ***

Authors’ reply

Sir

We agree with Lohiya RV that diabetes may affect the Duke treadmill score (DTS), and diabetics may have a misleadingly low-risk DTS for any given coronary artery disease burden. [1] Nevertheless, it does not seem probable with our study. There is only a numerical difference between Group I (moderate to high risk DTS) and Group II (low risk DTS) in terms of diabetes, and this difference is not statistically significant (P = 0.399). Furthermore, after adjustment for the presence of diabetes, the relationship of HDL cholesterol with DTS maintained its significance (r = 0.223, P = 0.030). In conclusion, the presence of diabetes should always be taken into account when interpreting the DTS.

Erkan AF, Ekici B, Demir GG, Töre HF

Department of Cardiology, Ufuk University, Ankara, Turkey Address for correspondence:

Dr. Berkay Ekici, E-mail: berkay.ekici@gmail.com

Reference

1. Lohiya RV. Duke’s treadmill score in diabetics-does it really matter? J Postgrad Med 2014;60:418.

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Journal of Postgraduate Medicine October 2014 Vol 60 Issue 4 419 

Letter to Editor Access this article online

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Dengue infection and acute

hypokalemic quadriparesis

Sir,

The case report on “Dengue infection and acute hypokalemic quadriparesis” is very interesting.[1] This condition is a rare dengue presentation and sporadically reported.[1-4] However, it should be noted that there are several possible causes of acute hypokalemic quadriparesis and it could simply be a co-morbidity associated with dengue. In this particular case, the over the counter use of acetaminophen and non steroidal anti inflammatory drugs is a confounder as these drugs can lead to renal dysfunction and consequent hypokalemic quadriparesis.[5]

Joob B, Wiwanitkit V1

Department of Sanitary, Medical Academic Center, Bangkok, Thailand, 1Hainan Medical University, China

Address for correspondence: Dr. Beuy Joob, E-mail: beuyjoob@hotmail.com

References

1. Gupta N, Garg A, Chhabra P. Dengue infection presenting as acute hypokalemic quadriparesis. J Postgrad Med 2014; 60:327-8.

2. Gutch M, Agarwal A, Amar A. Hypokalemic quadriparesis: An unusual manifestation of dengue fever. J Nat Sci Biol Med 2012;3:81-3.

3. Gupta DK, Vaish AK, Arya RK, Chaudhary SC. Hypokalaemic quadriparesis: An unusual manifestation of dengue fever. BMJ Case Rep 2011;2011. pii: bcr1220103673.

4. Jha S, Ansari MK. Dengue infection causing acute hypokalemic quadriparesis. Neurol India 2010;58:592-4.

5. Gaul C, Heckmann JG, Druschky A, Schöcklmann H, Neundörfer B, Erbguth F. Renal tubular acidosis with severe hypokalemic tetraparesis after ibuprofen intake. Dtsch Med Wochenschr 1999;124:483-6.

Access this article online Quick Response Code: Website:

www.jpgmonline.com DOI: 10.4103/0022-3859.143996 PubMed ID: ***

Dengue-related hypokalemic

paralysis-more questions than

answers

Sir,

We read the article by Gupta, et al.[1] with interest. Recent reports have revealed that the dengue virus (DENV), otherwise thought to be non neurotropic, exhibits neurotropism. This in turn reflects the changing clinical spectrum of dengue infection. Dengue-related hypokalemic paralysis is an emerging neuromuscular complication, and warrants special citation, in view of its rapidly evolving course, and excellent response to minimal potassium supplementation. Unfortunately it is mistaken with other entities causing rapidly progressive quadriparesis.[2]

Interestingly, until now dengue-related hypokalemic paralysis was attributed to redistribution of potassium or an increased loss from the body. It is mostly reported from northern parts of India, whereas similar findings were not reported from dengue prevalent tropical and sub-tropical countries. It is interesting to note that only few patients had manifested quadriparesis when more than two-thirds exhibited hypokalemia.[3] This observation provokes important questions about the geographical variation and whether the incidence has something to do with the genetic susceptibility. The pathophysiology behind the development of hypokalemic paralysis in these patients is not well understood and we highlight here molecular mechanisms and the importance of recognizing such entities. Hypokalemic periodic paralysis has been shown to be precipitated by mutations in the two skeletal muscle genes imparting susceptibility to the affected patients. Is it possible that patients with dengue-related hypokalemic quadriparesis have some kind of channelopathy contributing to their susceptibility to develop paralysis similar to what has been observed in hypokalemic periodic paralysis?

The occurrence of dengue related - hypokalemic paralysis/ quadriparesis in a limited number of cases makes one recall factors related to DENV and host cellular response. Is it possible that serotypes of DENV and/ or their effects on dengue-sensitized individual host cell membrane, intra-cellular organelle, mitochondrial dynamics or immune signaling would have contributed to the development of hypokalemia paralysis? Such cases must be reassured and provided with dietary modifications, and educated to consult their practitioners, if they develop weakness following viral fever. Also, the practitioners should be made to realize and distinguish post infectious hypokalemic paralysis from other acute flaccid paralysis or Guillain-Barre syndromes. The possibility of the recurrence of paralysis following overt or covert infection in one and the same individual again has to be remembered and informed. Such cases require further studies so as to ascertain the underlying mechanisms in terms of prevention and therapy.

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