|Year : 2014 | Volume
| Issue : 1 | Page : 35-37
Pellagra and hypothyroidism: A rare combination
Arvind Bamanikar, Swati Dhobale
Department of Medicine, Padmashree Dr. D. Y Patil Medical College, Hospital and Research Center, Pune, Maharashtra, India
|Date of Web Publication||2-Jan-2014|
Department of Medicine, Padmashree Dr. D. Y Patil Medical College, Hospital and Research Center, Pune, Maharashtra
Source of Support: None, Conflict of Interest: None
Pellagra is more common in developing countries than the rest of the world. Malnutrition is more common in these countries; in part because the staple grains do not have sufficient niacin. Classical triad of diarrhoea, dermatitis, and dementia is diagnostic of pellagra. Milder forms can present with slowing of mental functions and skin manifestations can start as dryness of skin Castle's necklace and glove; stocking pattern of dermatitis. We had a female patient who was operated for thyroid disease in the past but was not on replacement therapy. Hypothyroidism and pellagra were diagnosed to be present simultaneously, which is reported very rarely. Both the conditions presenting concurrently may be incidental or could share the common metabolic pathway for becoming clinically overt. It is difficult to determine if the deficiency of vitamin B 3 which unmasked the thyroid deficiency or vice versa.
Keywords: Dermatitis, hypothyroidism, pellagra
|How to cite this article:|
Bamanikar A, Dhobale S. Pellagra and hypothyroidism: A rare combination. Thyroid Res Pract 2014;11:35-7
| Introduction|| |
Pellagra is present worldwide but more common in developing countries. Malnutrition is single important responsible factor; in part because the staple grains do not have sufficient niacin. In the 20 th century, pellagra has been common in Egypt and parts of southern and eastern Africa, and sporadic cases have been reported in India. In each of these areas, the disease was associated with maize as the staple diet of poor people who could afford very little else to supplement the diet. An erythematous, blistering rash as well as glossitis, stomatitis may be seen more commonly than other clinical features in pellagra. Patients may have neurologic manifestations such as disorientation, muscular weakness (especially of the lower extremities), myoclonic jerks, tremors, insomnia, fatigue, depression, and central pontine myelinolysis. Nausea, vomiting, and/or diarrhoea often precede the other manifestations. Risk factors for developing pellagra include poverty, staple diet poor in niacin (maize, Indian millet, or jowar), eating disorders, alcohol abuse, malabsorption, medication (Isoniazid, pyrazinamide, carbamazepine, carbidopa, chloramphenicol, phenytoin, phenobarbital), chemotherapy (5-fluorouracil, 6-mercaptopurine, azathioprine), postsurgical complications (gastrectomy), carcinoid syndrome, Crohn's disease, Hartnup disease, and hypothyroidism  .
Myxoedema pellagra has been reported in literature but it is very rare. ,,, We describe a case of hypothyroidism and pellagra occurred simultaneously and hypothyroid state was apparently unmasked by pellagra.
| Case Report|| |
Thirty-five-year-old Indian female presented with skin rash of 10 days duration and puffiness of face, swelling all over the body of 3 month duration. Patient noticed hyperpigmented lesions over extensor aspect of elbows, shins, face, and neck. The rash was scaly with dry skin and patient experienced burning sensation over these lesions. She had decreased appetite in last 1 month of illness. The swelling over the face and limbs did not have diurnal variation and she denied of any pain over the swollen areas. She had decreased appetite in last one month of illness. She also complained of breathlessness on exertion, gradually progressed from grade II to grade III New York Heart Association over 3-month period. She also experienced difficulty in performing her daily activities and also had fatigue after routine work at home. She had a few episodes of palpitations since last 15 days. The palpitations were brought on by exertion and disappeared after rest. She also complained of chest pain precipitated by exertion and relieved by rest. The pain was felt over the precordium, not radiating to left arm or neck and was not related to posture or respiration. She also complained of hoarseness of voice and diffuse hair loss since 1 month. There was no history of fever, orthoponea, paroxysmal nocturnal dyspnea, or postural dizziness. She had thyroidectomy 12 years ago for multinodular goiter but was not on thyroxin replacement or any other medication. There was no history of travel or stay in endemic areas for filariasis. She did not have history of kidney disease, hypertension, or diabetes. She had no bowel or bladder complaints and her menstrual cycle was regular with normal flow.
On examination, her face appeared puffy, dryness of skin was hvident all over the body [Figure 1]. She had masklike face with hoarse voice and slurred, but low tone monotonous speech. Her response time to general questions was slow. The pulse rate was 60/min, blood pressure was 120/80 mm Hg, respiratory rate was 24/min and she was not breathless at rest. Examination of tongue, oral cavity, and pharynx was normal. She had pallor, periorbital puffiness, and nonpitting edema on the legs. Scalp showed diffuse thinning of hair. She had multiple hyperpigmented ill-defined plaques over the neck with icthyotic plaques over extensor aspect of both upper limb and lower limbs [Figure 2]. The scar of thyroid surgery was noted. Body mass index was 29 with weight of 62 kg.
Systemic examination was normal, neurological examination revealed for delayed relaxation of ankle jerks. Investigations revealed haemoglobin 7.2 g/dL, platelet count 2, 60,000/cumm, microcytic hypochromic red cells. Total leucocyte count was 5800/cumm; Erythrocyte sedimentation rate was 50 mm in 1 st hour. Red cell indices showed mean corpuscular volume 77.9, mean corpuscular haemoglobin 24.2 pg/dL, mean corpuscular haemoglobin concentration 31.0 g/dL, hematocrit was 23.2%. S. cholesterol was 290 mg/dL (N = 160) S. triglycerides was 256 mg/dL (N = <150), S. high-density lipoprotein was 36 mg/dL, low-density lipoprotein was 148 mg/dL. Fasting blood glucose was 100 mg/dL with HbA 1 C 7.9. Biochemical parameters for liver and kidney functions tests were normal. Serum iron studies (ferritin, transferrin, and total iron binding capacity) were consistent with iron deficiency anemia. Serum sodium and potassium values were 139 and 4.4 mmol/L, respectively. The creatinine phosphokinase was 24 IU/L. Urine routine examination was normal. Her electrocardiography revealed heart rate of 60/min with low voltage. Her thyroid function test showed thyroid stimulating hormone >150 μIU/L (N: 0.30-5.5), free T 3 (triiodothyronine) 0.51 pg/mL (N: 1.7-4.2), free thyroxin (T 4 ) of 0.08 (N: 0.70-1.80) diagnostic of primary hypothyroidism. Two-dimensional echocardiography revealed minimal pericardial effusion. The systolic and diastolic functions were normal. Left ventricular ejection fraction was 60%. Grade I fatty liver detected on abdominal ultrasound.
Hypothyroidism with pellagra and iron deficiency anemia (nutritional) was the diagnosis. The urine test for levels of niacin was not available and is more useful to rule out niacin deficiency rather than a tool for diagnosis of pellagra. Patient was started on niacin 375 mg twice a day, thyroxin 75 mcg/day, and frusemide 20 mg/day; all given orally. Inj cobadex forte; containing folic Acid, vitamin B 1 , vitamin B 12 , vitamin B 2 , vitamin B 3 , vitamin B 5 , vitamin B 6 , vitamin C was given daily. She was also given 1000 mg of intravenous infusion of ferric carboxy maltose over a period of 30 min to replenish body iron stores. Patient showed remarkable improvement in skin and neurologic signs and symptoms within one week of treatment. Anaemia started improving. She was followed-up on outpatient basis and achieved remarkable improvement in anemia, pellagra, hypothyroid state within a month.
| Discussion|| |
Pellagra is due to niacin deficiency. The deficiency could be primarily nutritional in origin or secondary to other diseases Nicotinic acid is stored in the liver adequately and clinical features of pellagra set in only, if there is a chronic and prolonged depletion, experimentally. Pellagra has been induced after 2 months of a niacin-deficient diet; death will occur in 4-5 years if left untreated.  Our patient had the classical features of hypothyroidism and pellagra. Pellagra appeared to be due nutritional deficiency in our patient. in our patient. Patient had thyroid surgery but was not on replacement therapy. After 12 years of lack of hormonal supply, the subclinical hypothyroid state was unmasked most probably due to niacin deficiency. The cooccurrence of iron deficiency anemia suggested the prolonged nutritional deficiency could the factor responsible for pellagra and hypothyroidism could have an additional contributory role by way of impairment of flavoprotein pathway. At the outset, it appears that the onset of pellagra coincided with the onset of clinical hypothyroidism in our patient. The diagnosis of hypothyroidism was confirmed by the laboratory tests and pellagra was confirmed on clinical manifestations coupled with quick therapeutic response to niacin. Hypothyroidism can rarely produce pellagra through the flavoprotein system. , This pathogenesis is associated with riboflavin deficiency for the rare association with hypothyroidism. There are a very few previous reports on this interesting combination of pellagra and hypothyroidism. The hypothyroid state has been considered as etiological factor. However, there is no report of pellagra-inducing hypothyroidism. Nicotinamide Adenine Dinucleotide, Hydrogen-a reduced form plays essential roles in energy metabolism in the living cell. Severe lack of niacin causes the deficiency disease pellagra, whereas a mild deficiency slows down the metabolism, which may be a potential contributing factor toward unmasking of subclinical hypothyroid state.
| Acknowledgment|| |
Authors are grateful to residents in medicine for their help in clinical photographs.
| References|| |
|1.||Available from: http://see.visualdx.com/diagnosis/pellagra [Last accessed on 2013 Jun 24]. |
|2.||Biswas R, Irfan O, Dubey A, Khare A, Bansal S. Skin lesions with scanning speech and memory loss. BMJ Case Rep 2009: bcr07.2008.0487. [Last accesed on Mar 17, 2009]. |
|3.||Prasad PV, Babu A, Paul EK, Balasubramaniyan S. Myxoedema pellagra-a report of two cases. J Assoc Physicians India 2003;51:421-2. |
|4.||Kaur S, Kumar B, Mehta SK, Sharma SC, Naik SR, Dash RJ. Hypothyroidism associated with pellagra: Report of two cases. Bull Postgrad Inst Med Educ Res Chandigarh 1980;14:90-4. |
|5.||Desai SG, Wali GM. Myxoedema conditioned pellagra. J Indian Med Assoc 1982;78:145-7. |
|6.||Miller SJ. Nutritional deficiency and the skin. J Am Acad Dermatol 1989;21:1-30. |
|7.||Rivlin RS. Regulation of flavoprotein enzymes in hypothyroidism and in riboflavin deficiency. Adv Enzyme Regul 1970;8:239-50. |
[Figure 1], [Figure 2]