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 Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 13  |  Issue : 1  |  Page : 33-35

A rare association of Henoch–Schönlein purpura and autoimmune thyroidits


Department of Medicine, Era's Lucknow Medical College, Sarfarazganj, Lucknow, Uttar Pradesh, India

Date of Web Publication5-Jan-2016

Correspondence Address:
Ritu Karoli
Department of Medicine, Era's Lucknow Medical College, Sarfarazganj, Hardoi Road, Lucknow - 226 003, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-0354.157916

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  Abstract 

Poor compliance is the most common cause of elevated thyroid-stimulating hormone in patients with hypothyroidism who are on levothyroxine replacement. We present an interesting report of a patient who was a known case of primary hypothyroidism and had been euthyroid for more than 5 years on 75 μg daily levothyroxine, suddenly became grossly hypothyroid and diagnosed to have Henoch–Schönlein purpura (HSP) with nephritis.

Keywords: Autoimmune thyroidits, henoch–Schönlein purpura, levothyroxine


How to cite this article:
Siddiqi Z, Karoli R, Fatima J, Waris AA. A rare association of Henoch–Schönlein purpura and autoimmune thyroidits. Thyroid Res Pract 2016;13:33-5

How to cite this URL:
Siddiqi Z, Karoli R, Fatima J, Waris AA. A rare association of Henoch–Schönlein purpura and autoimmune thyroidits. Thyroid Res Pract [serial online] 2016 [cited 2019 Jun 15];13:33-5. Available from: http://www.thetrp.net/text.asp?2016/13/1/33/157916


  Introduction Top


Poor compliance is the most common cause of elevated thyroid-stimulating hormone in patients with hypothyroidism who are on levothyroxine replacement. There are certain clinical situations such as pregnancy or diseases like malabsorption syndromes and nephrotic syndrome or simultaneous intake of medications interfering with absorption or increasing metabolism of levothyroxine that can lead to increase in its requirement. There are occasional case reports of autoimmune thyroid diseases and Henoch–Schönlein purpura (HSP).[1] Hereby, we present report of a patient who was a known case of primary hypothyroidism and had been euthyroid for more than5 years on 75 µg daily levothyroxine, suddenly became grossly hypothyroid and diagnosed to have HSP with nephritis.


  Case Report Top


A 36-year-old female from rural background was admitted in our hospital with a month long history of oliguria, severe constipation, pitting edema, and skin eruptions over both legs. This was preceded by an episode of fever and cough with expectoration lasting for a week. She had no previous medical history of chronic illnesses except hypothyroidism. There was no history or clinical evidence of malabsorption syndrome, pancreatitis, or short bowel syndrome. Any current use of medications such as antacids, calcium, cholestyramine, or iron preparations was excluded. At the time of presentation she was on 200 µg of levothyroxine replacement with reportedly good compliance. Her family history was unremarkable. General examination was normal except presence of pallor, dry skin, hoarse voice, and multiple nontender purpura mixed with erythema ranging from 2 to 5 mm in diameter over her legs [Figure 1]. Most of the skin lesions were nonindurated, although palpable or indurated purpura mixed with erythema could be identified in some areas. Systemic examination did not reveal any abnormality. On admission, laboratory investigations showed hemoglobin level of 8 g/dL with microcytic hypochromic peripheral blood smear. There was elevated serum creatinine level of 2.4 mg/dL, an increased blood urea nitrogen level of 56 mg/dL, urine red blood cell (RBC) 25–30/HPF, and 24-h urine protein 5.6g/day. Her C3 was low while vasculitis workup including rheumatoid factor (RF), antinuclear antibody (ANA), antineutrophil cytoplasmic antibodies (ANCAs), and anti-double stranded deoxyribonucleic acid (dsDNA) was negative. Renal ultrasonography showed diffuse parenchymal swelling and homogenous increased cortical echogenicity with maintained corticomedulary differentiation. The histopathology report of skin rash was consistent with HSP. She was positive for thyroid peroxidase (TPO) antibodies (690 mIU/ml, normal < 100) with thyroid-stimulating hormone level 56 mIU/dl despite taking levothyroxine 200 µg daily on an empty stomach. Renal biopsy was suggestive of immunoglobulin A (Ig A) nephropathy [Figure 2]. We started with oral prednisolone 60 mg daily. Starting steroid therapy, her renal parameters and proteinuria were improved. After 6 weeks, her levothyroxine requirement was also reduced to 150 µg. At present she is doing well.
Figure 1: Multiple nontender palpable purpura mixed with erythema

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Figure 2: Renal biopsy with immunofluorescence stain suggestive of immunoglobulin A (IgA) nephropathy

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  Discussion Top


Henoch-Schönlein purpura (HSP) is a systemic vasculitis involving small vessels with the deposition of immune complexes containing IgA in renal mesangium and blood vessels. Clinical manifestations show purpuric skin lesions, arthralgia, abdominal pain, bleeding, nephritis, neurologic involvement, and pulmonary hemorrhage. It is typically a disease of children and rare in adults. Nephritis is a severe complication of HSP that can proceed to end-stage renal failure, and its severity affects long-term prognosis. HSP nephritis (HSPN) and IgA nephropathy are currently considered related diseases, as both are indistinguishable in the renal histologic and immunofluorescent findings. HSPN more often shows extrarenal manifestation, nephritic-nephrotic syndrome, and chronic renal failure compared to IgA nephropathy.

There have been associations of several glomerulonephritides with hypothyroidism and Graves' disease. The proposed mechanisms for these associations can be immune complex deposition in the glomerular as well as thyroid epithelial basement membrane and the occurrence of autoimmune thyroid disease in association with other autoimmune diseases such as type 1 diabetes mellitus or HSP implicate a common autoimmune pathogenesis.

A linear relationship has been observed between proteinuria and urinary total tetraiodothyronine (T4) concentrations in patients with nephritic syndrome.[2] In patients with hypothyroidism taking levothyroxine who develop nephrotic syndrome are unable to compensate for urinary losses of T4, which results in increased requirement of levothyroxine in previously euthyroid patients.[3]

Thyroid function abnormalities, comprising urinary loss of thyroid-binding globulin (TBG), free T4, and free triiodothyronine (T3), with consequent falls in serum T4, T3, and TBG levels, are well-documented in children with untreated nephrotic syndrome and are reversible with disease remission or following bilateral nephrectomy and renal replacement therapy.[4],[5]


  Conclusion Top


To conclude, patients with primary thyroid failure on replacement who develop nephrotic syndromemay rarely present with anabrupt increase in levothyroxine requirements. In patients who already have one autoimmune disorder, we should always consider and search for presence of other organ-specific autoimmune diseases.

 
  References Top

1.
Garcia-Porrua C, Gonzalez-Gay MA, Botana M, Sanchez-Andrade A. Henoch–Scho¨nlein purpura in adults and autoimmune thyroiditis. J Rheumatol 2000;27:1326-7.  Back to cited text no. 1
    
2.
Chandurkar V, Shik J, Randell E. Exacerbation of underlying hypothyroidismcaused by proteinuria and induction of urinary thyroxine loss: Case report and subsequent investigation. Endocr Pract 2008;14:97-103.  Back to cited text no. 2
    
3.
Collins MT, Remaley AT, Csako G, Pucino F, Skarulis MC, Balow JE, et al. Increased levothyroxine requirements presenting as “inappropriate” TSH secretion syndrome in a patient with nephrotic syndrome. J Endocrinol Invest 2000;23:383-92.  Back to cited text no. 3
    
4.
Feinstein EI, Kaptein EM, Nicoloff JT, Massry SG. Thyroid function in patients with nephrotic syndrome and normal renal function. Am J Nephrol 1982;2:70-6.  Back to cited text no. 4
    
5.
Muranjan MN, Kher AS, Nadkarni UB, Kamat JR. Congenital nephrotic syndrome with clinical hypothyroidism. Indian J Pediatr1995;62:233-5.  Back to cited text no. 5
    


    Figures

  [Figure 1], [Figure 2]



 

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Abstract
Introduction
Case Report
Discussion
Conclusion
References
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